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堀江 稔

所属部署名内科学講座(循環器内科)
職名教授
 
 
更新日: 18/06/20 09:28

研究者基本情報

氏名

    堀江 稔

所属(マスタ)

  • 内科学講座(循環器内科) 教授

学歴

  • - 1988年京都大学 医学研究科
  • - 1978年京都大学 医学部

学位

  • 医学博士(京都大学)

所属学協会

    臨床電気生理研究会 , 日本睡眠学会 , 日本核医学会 , 日本糖尿病学会 , 日本生理学会 , 日本内科学会 , 日本心不全学会 , 日本不整脈心電学会 , 日本循環器学会

経歴

  • 1988年大学院医学研究科、1988年〜京大病院循環器内科勤務、2002年から現職
  • - 1984年1978年京都大学卒業、〜1984年まで市立静岡市民病院内科、〜1988年京都大学

研究活動情報

論文

  • Not all rotors, effective ablation targets for nonparoxysmal atrial fibrillation, are included in areas suggested by conventional indirect indicators of atrial fibrillation drivers: ExTRa Mapping project.
    Sakata K, Okuyama Y, Ozawa T, Haraguchi R, Nakazawa K, Tsuchiya T, Horie M, Ashihara T
    Journal of arrhythmia 34(2) 176-184 2018年04月 [査読有り]
  • Serum magnesium, phosphorus, and calcium levels and subclinical calcific aortic valve disease: A population-based study.
    Hisamatsu T, Miura K, Fujiyoshi A, Kadota A, Miyagawa N, Satoh A, Zaid M, Yamamoto T, Horie M, Ueshima H, SESSA Research Group.
    Atherosclerosis 273 145-152 2018年03月 [査読有り]
  • Copy number variations of SCN5A in Brugada syndrome.
    Sonoda K, Ohno S, Ozawa J, Hayano M, Hattori T, Kobori A, Yahata M, Aburadani I, Watanabe S, Matsumoto Y, Makiyama T, Horie M
    Heart rhythm 2018年03月 [査読有り]
  • Population pharmacokinetics and pharmacogenomics of apixaban in Japanese adult patients with atrial fibrillation.
    Ueshima S, Hira D, Kimura Y, Fujii R, Tomitsuka C, Yamane T, Tabuchi Y, Ozawa T, Itoh H, Ohno S, Horie M, Terada T, Katsura T
    British journal of clinical pharmacology 2018年02月 [査読有り]
  • A hERG mutation E1039X produced a synergistic lesion on IKs together with KCNQ1-R174C mutation in a LQTS family with three compound mutations.
    Wu J, Mizusawa Y, Ohno S, Ding WG, Higaki T, Wang Q, Kohjitani H, Makiyama T, Itoh H, Toyoda F, James AF, Hancox JC, Matsuura H, Horie M
    Scientific reports 8(1) 3129 2018年02月 [査読有り]
  • A challenge for mutation specific risk stratification in long QT syndrome type 1.
    Yagi N, Itoh H, Hisamatsu T, Tomita Y, Kimura H, Fujii Y, Makiyama T, Horie M, Ohno S
    Journal of cardiology 72(1) 56-65 2018年02月 [査読有り]
  • Bradycardia is a Specific Phenotype of Catecholaminergic Polymorphic Ventricular Tachycardia Induced by RYR2 Mutations.
    Miyata K, Ohno S, Itoh H, Horie M
    Internal medicine (Tokyo, Japan) 2018年02月 [査読有り]
  • Restoration of mutant hERG stability by inhibition of HDAC6.
    Li P, Kurata Y, Endang M, Ninomiya H, Higaki K, Taufiq F, Morikawa K, Shirayoshi Y, Horie M, Hisatome I
    Journal of molecular and cellular cardiology 115 158-169 2018年02月 [査読有り]
  • Association of Coronary Artery Calcification with Estimated Coronary Heart Disease Risk from Prediction Models in a Community-Based Sample of Japanese Men: The Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA).
    Tai Pham., Fujiyoshi A, Arima H, Tanaka-Mizuno S, Hisamatsu T, Kadowaki S, Kadota A, Zaid M, Sekikawa A, Yamamoto T, Horie M, Miura K, Ueshima H, Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA) Research Group.
    Journal of atherosclerosis and thrombosis 2017年12月 [査読有り]
  • Gene-Based Risk Stratification for Cardiac Disorders in LMNA Mutation Carriers.
    Nishiuchi S, Makiyama T, Aiba T, Nakajima K, Hirose S, Kohjitani H, Yamamoto Y, Harita T, Hayano M, Wuriyanghai Y, Chen J, Sasaki K, Yagihara N, Ishikawa T, Onoue K, Murakoshi N, Watanabe I, Ohkubo K, Watanabe H, Ohno S, Doi T, Shizuta S, Minamino T, Saito Y, Oginosawa Y, Nogami A, Aonuma K, Kusano K, Makita N, Shimizu W, Horie M, Kimura T
    Circulation. Cardiovascular genetics 10(6) 2017年12月 [査読有り]
  • Different responses to exercise between Andersen-Tawil syndrome and catecholaminergic polymorphic ventricular tachycardia.
    Inoue YY, Aiba T, Kawata H, Sakaguchi T, Mitsuma W, Morita H, Noda T, Takaki H, Toyohara K, Kanaya Y, Itoi T, Mitsuhashi T, Sumitomo N, Cho Y, Yasuda S, Kamakura S, Kusano K, Miyamoto Y, Horie M, Shimizu W
    Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology 2017年12月 [査読有り]
  • Refractory ventricular fibrillations after surgical repair of atrial septal defects in a patient with CACNA1C gene mutation - case report.
    Kojima A, Shikata F, Okamura T, Higaki T, Ohno S, Horie M, Uchita S, Kawanishi Y, Namiguchi K, Yasugi T, Izutani H
    Journal of cardiothoracic surgery 12(1) 118 2017年12月 [査読有り]
  • Unique genetic background and outcome of non-Caucasian Japanese probands with arrhythmogenic right ventricular dysplasia/cardiomyopathy.
    Wada Y, Ohno S, Aiba T, Horie M
    Molecular genetics & genomic medicine 5(6) 639-651 2017年11月 [査読有り]
  • Single-session versus staged procedures for elective multivessel percutaneous coronary intervention.
    Toyota T, Morimoto T, Shiomi H, Yamaji K, Ando K, Ono K, Shizuta S, Saito N, Kato T, Kaji S, Furukawa Y, Nakagawa Y, Kadota K, Horie M, Kimura T, CREDO-Kyoto PCI/CABG Registry Cohort-2 Investigators.
    Heart (British Cardiac Society) 104(11) 936-944 2017年11月 [査読有り]
  • Novel intracellular transport-refractory mutations in KCNH2 identified in patients with symptomatic long QT syndrome.
    Fukumoto D, Ding WG, Wada Y, Fujii Y, Ichikawa M, Takayama K, Fukuyama M, Kato K, Itoh H, Makiyama T, Omatsu-Kanbe M, Matsuura H, Horie M, Ohno S
    Journal of cardiology 71(4) 401-408 2017年11月 [査読有り]
  • Macro-pro-B-type natriuretic peptide (proBNP) and hidden macro-N-terminal proBNP: Case report.
    Nakagawa Y, Nishikimi T, Sakai H, Ohno S, Kinoshita H, Inazumi H, Moriuchi K, Kuwahara K, Horie M, Kimura T
    Clinical biochemistry 52 148-152 2017年11月 [査読有り]
  • The relationship between J waves and contact of lung cancer with the heart.
    Hayashi H, Wu Q, Horie M
    Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc 22(5) 2017年09月 [査読有り]
  • Arrhythmia risk and β-blocker therapy in pregnant women with long QT syndrome.
    Ishibashi K, Aiba T, Kamiya C, Miyazaki A, Sakaguchi H, Wada M, Nakajima I, Miyamoto K, Okamura H, Noda T, Yamauchi T, Itoh H, Ohno S, Motomura H, Ogawa Y, Goto H, Minami T, Yagihara N, Watanabe H, Hasegawa K, Terasawa A, Mikami H, Ogino K, Nakano Y, Imashiro S, Fukushima Y, Tsuzuki Y, Asakura K, Yoshimatsu J, Shiraishi I, Kamakura S, Miyamoto Y, Yasuda S, Akasaka T, Horie M, Shimizu W, Kusano K
    Heart (British Cardiac Society) 103(17) 1374-1379 2017年09月 [査読有り]
  • Impact of ABCB1, ABCG2, and CYP3A5 polymorphisms on plasma trough concentrations of apixaban in Japanese patients with atrial fibrillation.
    Ueshima S, Hira D, Fujii R, Kimura Y, Tomitsuka C, Yamane T, Tabuchi Y, Ozawa T, Itoh H, Horie M, Terada T, Katsura T
    Pharmacogenetics and genomics 27(9) 329-336 2017年09月 [査読有り]
  • Drug-induced fatal arrhythmias: Acquired long QT and Brugada syndromes.
    Turker I, Ai T, Itoh H, Horie M
    Pharmacology & therapeutics 176 48-59 2017年08月 [査読有り]
  • Heart failure in patients with arrhythmogenic right ventricular cardiomyopathy: What are the risk factors?
    Kimura Y, Noda T, Matsuyama TA, Otsuka Y, Kamakura T, Wada M, Ishibashi K, Inoue Y, Miyamoto K, Okamura H, Nagase S, Aiba T, Kamakura S, Noguchi T, Anzai T, Satomi K, Wada Y, Ohno S, Horie M, Shimizu W, Yasuda S, Shimokawa H, Kusano K
    International journal of cardiology 241 288-294 2017年08月 [査読有り]
  • Long QT syndrome presents not only as QT prolongation but also as abnormal T-wave morphology.
    Horie M
    Heart rhythm 14(8) 1171-1172 2017年08月 [査読有り]
  • Self-reported Sleep Duration and Subclinical Atherosclerosis in a General Population of Japanese Men.
    Suzuki S, Arima H, Miyazaki S, Fujiyoshi A, Kadota A, Takashima N, Hisamatsu T, Kadowaki S, Zaid M, Torii S, Horie M, Murata K, Miura K, Ueshima H, SESSA Research Group.
    Journal of atherosclerosis and thrombosis 25(2) 186-198 2017年07月 [査読有り]
  • Progressive Atrial Conduction Defects Associated With Bone Malformation Caused by a Connexin-45 Mutation.
    Seki A, Ishikawa T, Daumy X, Mishima H, Barc J, Sasaki R, Nishii K, Saito K, Urano M, Ohno S, Otsuki S, Kimoto H, Baruteau AE, Thollet A, Fouchard S, Bonnaud S, Parent P, Shibata Y, Perrin JP, Le Marec H, Hagiwara N, Mercier S, Horie M, Probst V, Yoshiura KI, Redon R, Schott JJ, Makita N
    Journal of the American College of Cardiology 70(3) 358-370 2017年07月 [査読有り]
  • Incidence and Prognostic Impact of Heart Failure Hospitalization During Follow-Up After Primary Percutaneous Coronary Intervention in ST-Segment Elevation Myocardial Infarction.
    Taniguchi T, Shiomi H, Morimoto T, Watanabe H, Ono K, Shizuta S, Kato T, Saito N, Kaji S, Ando K, Kadota K, Furukawa Y, Nakagawa Y, Horie M, Kimura T
    The American journal of cardiology 119(11) 1729-1739 2017年06月 [査読有り]
  • Genotype-Phenotype Correlation of SCN5A Mutation for the Clinical and Electrocardiographic Characteristics of Probands With Brugada Syndrome: A Japanese Multicenter Registry.
    Yamagata K, Horie M, Aiba T, Ogawa S, Aizawa Y, Ohe T, Yamagishi M, Makita N, Sakurada H, Tanaka T, Shimizu A, Hagiwara N, Kishi R, Nakano Y, Takagi M, Makiyama T, Ohno S, Fukuda K, Watanabe H, Morita H, Hayashi K, Kusano K, Kamakura S, Yasuda S, Ogawa H, Miyamoto Y, Kapplinger JD, Ackerman MJ, Shimizu W
    Circulation 135(23) 2255-2270 2017年06月 [査読有り]
  • Development of a Patient-Derived Induced Pluripotent Stem Cell Model for the Investigation of SCN5A-D1275N-Related Cardiac Sodium Channelopathy.
    Hayano M, Makiyama T, Kamakura T, Watanabe H, Sasaki K, Funakoshi S, Wuriyanghai Y, Nishiuchi S, Harita T, Yamamoto Y, Kohjitani H, Hirose S, Yokoi F, Chen J, Baba O, Horie T, Chonabayashi K, Ohno S, Toyoda F, Yoshida Y, Ono K, Horie M, Kimura T
    Circulation journal : official journal of the Japanese Circulation Society 81(12) 1783-1791 2017年06月 [査読有り]
  • Allele-specific ablation rescues electrophysiological abnormalities in a human iPS cell model of long-QT syndrome with a CALM2 mutation.
    Yamamoto Y, Makiyama T, Harita T, Sasaki K, Wuriyanghai Y, Hayano M, Nishiuchi S, Kohjitani H, Hirose S, Chen J, Yokoi F, Ishikawa T, Ohno S, Chonabayashi K, Motomura H, Yoshida Y, Horie M, Makita N, Kimura T
    Human molecular genetics 26(9) 1670-1677 2017年05月 [査読有り]
  • J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge.
    Antzelevitch C, Yan GX, Ackerman MJ, Borggrefe M, Corrado D, Guo J, Gussak I, Hasdemir C, Horie M, Huikuri H, Ma C, Morita H, Nam GB, Sacher F, Shimizu W, Viskin S, Wilde AAM
    Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology 19(4) 665-694 2017年04月 [査読有り]
  • Quantitative analysis of PKP2 and neighbouring genes in a patient with arrhythmogenic right ventricular cardiomyopathy caused by heterozygous PKP2 deletion.
    Sonoda K, Ohno S, Otuki S, Kato K, Yagihara N, Watanabe H, Makiyama T, Minamino T, Horie M
    Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology 19(4) 644-650 2017年04月 [査読有り]
  • Guidelines for Therapeutic Drug Monitoring of Cardiovascular Drugs Clinical Use of Blood Drug Concentration Monitoring (JCS 2015) - Digest Version.
    Aonuma K, Shiga T, Atarashi H, Doki K, Echizen H, Hagiwara N, Hasegawa J, Hayashi H, Hirao K, Ichida F, Ikeda T, Maeda Y, Matsumoto N, Sakaeda T, Shimizu W, Sugawara M, Totsuka K, Tsuchishita Y, Ueno K, Watanabe E, Hashiguchi M, Hirata S, Kasai H, Matsumoto Y, Nogami A, Sekiguchi Y, Shinohara T, Sugiyama A, Sumitomo N, Suzuki A, Takahashi N, Yukawa E, Homma M, Horie M, Inoue H, Ito H, Miura T, Ohe T, Shinozaki K, Tanaka K, Japanese Circulation Society and the Japanese Society of Therapeutic Drug Monitoring Joint Working Group.
    Circulation journal : official journal of the Japanese Circulation Society 81(4) 581-612 2017年03月 [査読有り]
  • Ad hoc vs. Non-ad hoc Percutaneous Coronary Intervention Strategies in Patients With Stable Coronary Artery Disease.
    Toyota T, Morimoto T, Shiomi H, Ando K, Ono K, Shizuta S, Kato T, Saito N, Furukawa Y, Nakagawa Y, Horie M, Kimura T, CREDO-Kyoto PCI/CABG Registry Cohort-2 Investigators.
    Circulation journal : official journal of the Japanese Circulation Society 81(4) 458-467 2017年03月 [査読有り]
  • Flecainide ameliorates arrhythmogenicity through NCX flux in Andersen-Tawil syndrome-iPS cell-derived cardiomyocytes.
    Kuroda Y, Yuasa S, Watanabe Y, Ito S, Egashira T, Seki T, Hattori T, Ohno S, Kodaira M, Suzuki T, Hashimoto H, Okata S, Tanaka A, Aizawa Y, Murata M, Aiba T, Makita N, Furukawa T, Shimizu W, Kodama I, Ogawa S, Kokubun N, Horigome H, Horie M, Kamiya K, Fukuda K
    Biochemistry and biophysics reports 9 245-256 2017年03月 [査読有り]
  • Cardiac conduction defects and Brugada syndrome: A family with overlap syndrome carrying a nonsense SCN5A mutation.
    Aoki H, Nakamura Y, Ohno S, Makiyama T, Horie M
    Journal of arrhythmia 33(1) 35-39 2017年02月 [査読有り]
  • Extensive Ca2+ leak through K4750Q cardiac ryanodine receptors caused by cytosolic and luminal Ca2+ hypersensitivity.
    Uehara A, Murayama T, Yasukochi M, Fill M, Horie M, Okamoto T, Matsuura Y, Uehara K, Fujimoto T, Sakurai T, Kurebayashi N
    The Journal of general physiology 149(2) 199-218 2017年01月 [査読有り]
  • Sick Sinus Syndrome with HCN4 Mutations Shows Early Onset and Frequent Association with Atrial Fibrillation and Left Ventricular Non-compaction.
    Ishikawa T, Ohno S, Murakami T, Yoshida K, Mishima H, Fukuoka T, Kimoto H, Sakamoto R, Ohkusa T, Aiba T, Nogami A, Sumitomo N, Shimizu W, Yoshiura KI, Horigome H, Horie M, Makita N
    Heart rhythm 14(5) 717-724 2017年01月 [査読有り]
  • Elimination of Ventricular Arrhythmia in Catecholaminergic Polymorphic Ventricular Tachycardia by Targeting "Catecholamine-sensitive area": A Dominant-Subordinate Relationship between Origin Sites of Bidirectional Ventricular Premature Contractions.
    Shirai Y, Goya M, Ohno S, Horie M, Doi S, Isobe M, Hirao K
    Pacing and clinical electrophysiology : PACE 40(5) 600-604 2016年12月 [査読有り]
  • Contribution of a KCNH2 variant in genotyped long QT syndrome: Romano-Ward syndrome under double mutations and acquired long QT syndrome under heterozygote.
    Fujii Y, Matsumoto Y, Hayashi K, Ding WG, Tomita Y, Fukumoto D, Wada Y, Ichikawa M, Sonoda K, Ozawa J, Makiyama T, Ohno S, Yamagishi M, Matsuura H, Horie M, Itoh H
    Journal of cardiology 70(1) 74-79 2016年11月 [査読有り]
  • Early repolarization and risk of arrhythmia events in long QT syndrome.
    Hasegawa K, Watanabe H, Hisamatsu T, Ohno S, Itoh H, Ashihara T, Hayashi H, Makiyama T, Minamino T, Horie M
    International journal of cardiology 223 540-542 2016年11月 [査読有り]
  • Phenotypic Variability of ANK2 Mutations in Patients With Inherited Primary Arrhythmia Syndromes.
    Ichikawa M, Aiba T, Ohno S, Shigemizu D, Ozawa J, Sonoda K, Fukuyama M, Itoh H, Miyamoto Y, Tsunoda T, Makiyama T, Tanaka T, Shimizu W, Horie M
    Circulation journal : official journal of the Japanese Circulation Society 80(12) 2442-2442 2016年10月 [査読有り]
  • Patient-Specific Human Induced Pluripotent Stem Cell Model Assessed with Electrical Pacing Validates S107 as a Potential Therapeutic Agent for Catecholaminergic Polymorphic Ventricular Tachycardia.
    Sasaki K, Makiyama T, Yoshida Y, Wuriyanghai Y, Kamakura T, Nishiuchi S, Hayano M, Harita T, Yamamoto Y, Kohjitani H, Hirose S, Chen J, Kawamura M, Ohno S, Itoh H, Takeuchi A, Matsuoka S, Miura M, Sumitomo N, Horie M, Yamanaka S, Kimura T
    PloS one 11(10) e0164795 2016年10月 [査読有り]
  • Genetics of Brugada syndrome.
    Juang JJ, Horie M
    Journal of arrhythmia 32(5) 425-425 2016年10月 [査読有り]
  • Molecular genetics have opened a new era for arrhythmia research, but also Pandora׳s box?
    Horie M
    Journal of arrhythmia 32(5) 313-314 2016年10月 [査読有り]
  • Molecular pathogenesis of long QT syndrome type 1.
    Wu J, Ding WG, Horie M
    Journal of arrhythmia 32(5) 388-388 2016年10月 [査読有り]
  • A type 2 ryanodine receptor variant associated with reduced Ca2+ release and short-coupled torsades de pointes ventricular arrhythmia.
    Fujii Y, Itoh H, Ohno S, Murayama T, Kurebayashi N, Aoki H, Blancard M, Nakagawa Y, Yamamoto S, Matsui Y, Ichikawa M, Sonoda K, Ozawa T, Ohkubo K, Watanabe I, Guicheney P, Horie M
    Heart rhythm : the official journal of the Heart Rhythm Society 14(1) 98-107 2016年10月 [査読有り]
  • J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge.
    Antzelevitch C, Yan GX, Ackerman MJ, Borggrefe M, Corrado D, Guo J, Gussak I, Hasdemir C, Horie M, Huikuri H, Ma C, Morita H, Nam GB, Sacher F, Shimizu W, Viskin S, Wilde AA
    Journal of arrhythmia 32(5) 339-339 2016年10月 [査読有り]
  • J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge.
    Antzelevitch C, Yan GX, Ackerman MJ, Borggrefe M, Corrado D, Guo J, Gussak I, Hasdemir C, Horie M, Huikuri H, Ma C, Morita H, Nam GB, Sacher F, Shimizu W, Viskin S, Wilde AA
    Heart rhythm 13(10) e295-e324 2016年10月 [査読有り]
  • LMNA cardiomyopathy detected in Japanese arrhythmogenic right ventricular cardiomyopathy cohort.
    Kato K, Takahashi N, Fujii Y, Umehara A, Nishiuchi S, Makiyama T, Ohno S, Horie M
    Journal of cardiology 68(4) 346-351 2016年10月 [査読有り]
  • Associations of serum LDL particle concentration with carotid intima-media thickness and coronary artery calcification.
    Zaid M, Miura K, Fujiyoshi A, Abbott RD, Hisamatsu T, Kadota A, Arima H, Kadowaki S, Torii S, Miyagawa N, Suzuki S, Takashima N, Ohkubo T, Sekikawa A, Maegawa H, Horie M, Nakamura Y, Okamura T, Ueshima H, SESSA Research Group.
    Journal of clinical lipidology 10(5) 1195-1202.e1 2016年09月 [査読有り]
  • Embryonic type Na+ channel β-subunit, SCN3B masks the disease phenotype of Brugada syndrome.
    Okata S, Yuasa S, Suzuki T, Ito S, Makita N, Yoshida T, Li M, Kurokawa J, Seki T, Egashira T, Aizawa Y, Kodaira M, Motoda C, Yozu G, Shimojima M, Hayashiji N, Hashimoto H, Kuroda Y, Tanaka A, Murata M, Aiba T, Shimizu W, Horie M, Kamiya K, Furukawa T, Fukuda K
    Scientific reports 6 34198 2016年09月 [査読有り]
  • Variants in the SCN5A Promoter Associated With Various Arrhythmia Phenotypes.
    Yagihara N, Watanabe H, Barnett P, Duboscq-Bidot L, Thomas AC, Yang P, Ohno S, Hasegawa K, Kuwano R, Chatel S, Redon R, Schott JJ, Probst V, Koopmann TT, Bezzina CR, Wilde AA, Nakano Y, Aiba T, Miyamoto Y, Kamakura S, Darbar D, Donahue BS, Shigemizu D, Tanaka T, Tsunoda T, Suda M, Sato A, Minamino T, Endo N, Shimizu W, Horie M, Roden DM, Makita N
    Journal of the American Heart Association 5(9) 2016年09月 [査読有り]
  • Significance of integrated in silico transmural ventricular wedge preparation models of human non-failing and failing hearts for safety evaluation of drug candidates.
    Kubo T, Ashihara T, Tsubouchi T, Horie M
    Journal of pharmacological and toxicological methods 83 30-41 2016年08月 [査読有り]
  • Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) Associated With Ryanodine Receptor (RyR2) Gene Mutations - Long-Term Prognosis After Initiation of Medical Treatment.
    Kawata H, Ohno S, Aiba T, Sakaguchi H, Miyazaki A, Sumitomo N, Kamakura T, Nakajima I, Inoue YY, Miyamoto K, Okamura H, Noda T, Kusano K, Kamakura S, Miyamoto Y, Shiraishi I, Horie M, Shimizu W
    Circulation journal : official journal of the Japanese Circulation Society 80(9) 1915-1915 2016年08月 [査読有り]
  • Smoking, Smoking Cessation, and Measures of Subclinical Atherosclerosis in Multiple Vascular Beds in Japanese Men.
    Hisamatsu T, Miura K, Arima H, Kadota A, Kadowaki S, Torii S, Suzuki S, Miyagawa N, Sato A, Yamazoe M, Fujiyoshi A, Ohkubo T, Yamamoto T, Murata K, Abbott RD, Sekikawa A, Horie M, Ueshima H, Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA) Research GroupNakanoYasutakaOgawaEmikoMaegawaHiroshiMiyazawaItsukoMitsunamiKenichiNozakiKazuhikoShiinoAkihikoArakiIsaoTsuruTeruhikoToyamaIkuoOgitaHisakazuKuritaSouichiMaedaToshinagaMiyamatsuNaomiKitaToruKimuraTakeshiNishioYoshihikoNakamuraYasuyukiOkamuraTomonoriBarinas‐MitchellEmma J.M.EdmundowiczDanielOhkuboTakayoshiHozawaAtsushiOkudaNagakoHigashiyamaAyaNagasawaShinyaKitaYoshikuniMurakamiYoshitakaTakashimaNaoyukiKadowakiTakash.
    Journal of the American Heart Association 5(9) 2016年08月 [査読有り]
  • Relationship of Insulin Resistance to Prevalence and Progression of Coronary Artery Calcification Beyond Metabolic Syndrome Components: Shiga Epidemiological Study of Subclinical Atherosclerosis.
    Yamazoe M, Hisamatsu T, Miura K, Kadowaki S, Zaid M, Kadota A, Torii S, Miyazawa I, Fujiyoshi A, Arima H, Sekikawa A, Maegawa H, Horie M, Ueshima H, SESSA Research Group.
    Arteriosclerosis, thrombosis, and vascular biology 36(8) 1703-1708 2016年08月 [査読有り]
  • Asymmetry of parental origin in long QT syndrome: preferential maternal transmission of KCNQ1 variants linked to channel dysfunction.
    Itoh H, Berthet M, Fressart V, Denjoy I, Maugenre S, Klug D, Mizusawa Y, Makiyama T, Hofman N, Stallmeyer B, Zumhagen S, Shimizu W, Wilde AA, Schulze-Bahr E, Horie M, Tezenas du Montcel S, Guicheney P
    European journal of human genetics : EJHG 24(8) 1160-1166 2016年08月 [査読有り]
  • Inter-Facility Transfer vs. Direct Admission of Patients With ST-Segment Elevation Acute Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.
    Nakatsuma K, Shiomi H, Morimoto T, Furukawa Y, Nakagawa Y, Ando K, Kadota K, Yamamoto T, Suwa S, Horie M, Kimura T, CREDO-Kyoto AMI investigators.
    Circulation journal : official journal of the Japanese Circulation Society 80(8) 1772-1772 2016年07月 [査読有り]
  • Comparison of circadian, weekly, and seasonal variations of electrical storms and single events of ventricular fibrillation in patients with Brugada syndrome.
    Aizawa Y, Takatsuki S, Kaneko Y, Noda T, Katsumata Y, Nishiyama T, Kimura T, Nishiyama N, Fukumoto K, Niwano S, Kurita T, Mitsuhashi T, Kamakura S, Shimizu A, Horie M, Aizawa Y, Fukuda K
    International journal of cardiology. Heart & vasculature 11 104-110 2016年06月 [査読有り]
  • The genetics underlying acquired long QT syndrome: impact for genetic screening.
    Itoh H, Crotti L, Aiba T, Spazzolini C, Denjoy I, Fressart V, Hayashi K, Nakajima T, Ohno S, Makiyama T, Wu J, Hasegawa K, Mastantuono E, Dagradi F, Pedrazzini M, Yamagishi M, Berthet M, Murakami Y, Shimizu W, Guicheney P, Schwartz PJ, Horie M
    European heart journal 37(18) 1456-1464 2016年05月 [査読有り]
  • Practical applicability of landiolol, an ultra-short-acting β1-selective blocker, for rapid atrial and ventricular tachyarrhythmias with left ventricular dysfunction.
    Wada Y, Aiba T, Tsujita Y, Itoh H, Wada M, Nakajima I, Ishibashi K, Okamura H, Miyamoto K, Noda T, Sugano Y, Kanzaki H, Anzai T, Kusano K, Yasuda S, Horie M, Ogawa H
    Journal of arrhythmia 32(2) 88-88 2016年04月 [査読有り]
  • Splicing misregulation of SCN5A contributes to cardiac-conduction delay and heart arrhythmia in myotonic dystrophy.
    Freyermuth F, Rau F, Kokunai Y, Linke T, Sellier C, Nakamori M, Kino Y, Arandel L, Jollet A, Thibault C, Philipps M, Vicaire S, Jost B, Udd B, Day JW, Duboc D, Wahbi K, Matsumura T, Fujimura H, Mochizuki H, Deryckere F, Kimura T, Nukina N, Ishiura S, Lacroix V, Campan-Fournier A, Navratil V, Chautard E, Auboeuf D, Horie M, Imoto K, Lee KY, Swanson MS, Lopez de Munain A, Inada S, Itoh H, Nakazawa K, Ashihara T, Wang E, Zimmer T, Furling D, Takahashi MP, Charlet-Berguerand N
    Nature communications 7 11067 2016年04月 [査読有り]
  • Lipoprotein-associated phospholipase A2 is related to risk of subclinical atherosclerosis but is not supported by Mendelian randomization analysis in a general Japanese population.
    Ueshima H, Kadowaki T, Hisamatsu T, Fujiyoshi A, Miura K, Ohkubo T, Sekikawa A, Kadota A, Kadowaki S, Nakamura Y, Miyagawa N, Okamura T, Kita Y, Takashima N, Kashiwagi A, Maegawa H, Horie M, Yamamoto T, Kimura T, Kita T, ACCESS and SESSA Research Groups.
    Atherosclerosis 246 141-147 2016年03月 [査読有り]
  • Evaluation and management of bradycardia in neonates and children.
    Baruteau AE, Perry JC, Sanatani S, Horie M, Dubin AM
    European journal of pediatrics 175(2) 151-161 2016年02月 [査読有り]
  • Efficacy of Antiarrhythmic Drugs Short-Term Use After Catheter Ablation for Atrial Fibrillation (EAST-AF) trial.
    Kaitani K, Inoue K, Kobori A, Nakazawa Y, Ozawa T, Kurotobi T, Morishima I, Miura F, Watanabe T, Masuda M, Naito M, Fujimoto H, Nishida T, Furukawa Y, Shirayama T, Tanaka M, Okajima K, Yao T, Egami Y, Satomi K, Noda T, Miyamoto K, Haruna T, Kawaji T, Yoshizawa T, Toyota T, Yahata M, Nakai K, Sugiyama H, Higashi Y, Ito M, Horie M, Kusano KF, Shimizu W, Kamakura S, Morimoto T, Kimura T, Shizuta S, EAST-AF Trial Investigators.
    European heart journal 37(7) 610-618 2016年02月 [査読有り]
  • Cardiac sodium channel mutation associated with epinephrine-induced QT prolongation and sinus node dysfunction.
    Chen J, Makiyama T, Wuriyanghai Y, Ohno S, Sasaki K, Hayano M, Harita T, Nishiuchi S, Yuta Yamamoto, Ueyama T, Shimizu A, Horie M, Kimura T
    Heart rhythm 13(1) 289-298 2016年01月 [査読有り]
  • High Frequency of Early Repolarization and Brugada-Type Electrocardiograms in Hypercalcemia.
    Sonoda K, Watanabe H, Hisamatsu T, Ashihara T, Ohno S, Hayashi H, Horie M, Minamino T
    Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc 21(1) 30-40 2016年01月 [査読有り]
  • A Novel SCN5A Mutation Associated with Drug Induced Brugada Type ECG.
    Turker I, Makiyama T, Vatta M, Itoh H, Ueyama T, Shimizu A, Ai T, Horie M
    PloS one 11(8) e0161872 2016年 [査読有り]
  • Association between Progressive Intraventricular Conduction Disturbance and Cardiovascular Events.
    Hayashi H, Wu Q, Horie M
    PloS one 11(7) e0157412 2016年 [査読有り]
  • Multigenerational Inheritance of Long QT Syndrome Type 2 in a Japanese Family.
    Ichikawa M, Ohno S, Fujii Y, Ozawa J, Sonoda K, Fukuyama M, Kato K, Kimura H, Itoh H, Hayashi H, Horie M
    Internal medicine (Tokyo, Japan) 55(3) 262-262 2016年 [査読有り]
  • Pediatric Cohort With Long QT Syndrome - KCNH2 Mutation Carriers Present Late Onset But Severe Symptoms.
    Ozawa J, Ohno S, Hisamatsu T, Itoh H, Makiyama T, Suzuki H, Saitoh A, Horie M
    Circulation journal : official journal of the Japanese Circulation Society 80(3) 702-702 2016年 [査読有り]
  • Intravascular Ultrasound Guidance vs. Angiographic Guidance in Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction - Long-Term Clinical Outcomes From the CREDO-Kyoto AMI Registry.
    Nakatsuma K, Shiomi H, Morimoto T, Ando K, Kadota K, Watanabe H, Taniguchi T, Yamamoto T, Furukawa Y, Nakagawa Y, Horie M, Kimura T, CREDO-Kyoto AMI investigators.
    Circulation journal : official journal of the Japanese Circulation Society 80(2) 477-484 2016年 [査読有り]
  • Culprit Vessel-Only vs. Staged Multivessel Percutaneous Coronary Intervention Strategies in Patients With Multivessel Coronary Artery Disease Undergoing Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction.
    Toyota T, Shiomi H, Taniguchi T, Morimoto T, Furukawa Y, Nakagawa Y, Horie M, Kimura T, CREDO-Kyoto AMI Registry Investigators.
    Circulation journal : official journal of the Japanese Circulation Society 80(2) 371-378 2016年 [査読有り]
  • Biphasic P wave in inferior leads and the development of atrial fibrillation.
    Hayashi H, Horie M
    Journal of arrhythmia 31(6) 376-380 2015年12月 [査読有り]
  • Adenosine triphosphate-guided pulmonary vein isolation for atrial fibrillation: the UNmasking Dormant Electrical Reconduction by Adenosine TriPhosphate (UNDER-ATP) trial.
    Kobori A, Shizuta S, Inoue K, Kaitani K, Morimoto T, Nakazawa Y, Ozawa T, Kurotobi T, Morishima I, Miura F, Watanabe T, Masuda M, Naito M, Fujimoto H, Nishida T, Furukawa Y, Shirayama T, Tanaka M, Okajima K, Yao T, Egami Y, Satomi K, Noda T, Miyamoto K, Haruna T, Kawaji T, Yoshizawa T, Toyota T, Yahata M, Nakai K, Sugiyama H, Higashi Y, Ito M, Horie M, Kusano KF, Shimizu W, Kamakura S, Kimura T, UNDER-ATP Trial Investigators.
    European heart journal 36(46) 3276-3287 2015年12月 [査読有り]
  • The association of J wave and ventricular tachycardia before device implantation with device interventions for ventricular tachyarrhythmia.
    Hayashi H, Horie M
    Journal of electrocardiology 48(4) 721-728 2015年07月 [査読有り]
  • Long-term outcomes associated with prolonged PR interval in the general Japanese population.
    Hisamatsu T, Miura K, Fujiyoshi A, Okamura T, Ohkubo T, Nagasawa SY, Horie M, Okayama A, Ueshima H, NIPPON DATA80 Research Group.
    Int J Cardiol 184(1) 291-293 2015年04月 [査読有り]
  • Efficacy and safety of flecainide for ventricular arrhythmias in patients with Andersen-Tawil syndrome with KCNJ2 mutations.
    Miyamoto K, Aiba T, Kimura H, Hayashi H, Ohno S, Yasuoka C, Tanioka Y, Tsuchiya T, Yoshida Y, Hayashi H, Tsuboi I, Nakajima I, Ishibashi K, Okamura H, Noda T, Ishihara M, Anzai T, Yasuda S, Miyamoto Y, Kamakura S, Kusano K, Ogawa H, Horie M, Shimizu W
    Heart rhythm 12(3) 596-603 2015年03月 [査読有り]
  • Löffler Endocarditis and Lacking Heart.
    Sawayama Y, Itoh H, Sakai H, Horie M
    Internal medicine (Tokyo, Japan) 54(23) 3093 2015年 [査読有り]
  • Association between Pulse Wave Velocity and Coronary Artery Calcification in Japanese men.
    Torii S, Arima H, Ohkubo T, Fujiyoshi A, Kadota A, Takashima N, Kadowaki S, Hisamatsu T, Saito Y, Miyagawa N, Zaid M, Murakami Y, Abbott RD, Horie M, Miura K, Ueshima H, SESSA Research Group.
    Journal of atherosclerosis and thrombosis 22(12) 1266-1277 2015年 [査読有り]
  • A Common Mutation of Long QT Syndrome Type 1 in Japan.
    Itoh H, Dochi K, Shimizu W, Denjoy I, Ohno S, Aiba T, Kimura H, Kato K, Fukuyama M, Hasagawa K, Schulze-Bahr E, Guicheney P, Horie M
    Circulation journal : official journal of the Japanese Circulation Society 79(9) 2026-2030 2015年 [査読有り]
  • Gender Differences in the Inheritance Mode of RYR2 Mutations in Catecholaminergic Polymorphic Ventricular Tachycardia Patients.
    Ohno S, Hasegawa K, Horie M
    PloS one 10(6) e0131517 2015年 [査読有り]
  • Clinical and Pathological Impact of Tissue Fibrosis on Lethal Arrhythmic Events in Hypertrophic Cardiomyopathy Patients With Impaired Systolic Function.
    Wada Y, Aiba T, Matsuyama TA, Nakajima I, Ishibashi K, Miyamoto K, Yamada Y, Okamura H, Noda T, Satomi K, Morita Y, Kanzaki H, Kusano K, Anzai T, Kamakura S, Ishibashi-Ueda H, Shimizu W, Horie M, Yasuda S, Ogawa H
    Circulation journal : official journal of the Japanese Circulation Society 79(8) 1733-1741 2015年 [査読有り]
  • Electrical storm in patients with brugada syndrome is associated with early repolarization.
    Kaneko Y, Horie M, Niwano S, Kusano KF, Takatsuki S, Kurita T, Mitsuhashi T, Nakajima T, Irie T, Hasegawa K, Noda T, Kamakura S, Aizawa Y, Yasuoka R, Torigoe K, Suzuki H, Ohe T, Shimizu A, Fukuda K, Kurabayashi M, Aizawa Y
    Circulation. Arrhythmia and electrophysiology 7(6) 1122-1128 2014年12月 [査読有り]
  • Circadian pattern of fibrillatory events in non-Brugada-type idiopathic ventricular fibrillation with a focus on J waves.
    Aizawa Y, Sato M, Ohno S, Horie M, Takatsuki S, Fukuda K, Chinushi M, Usui T, Aonuma K, Hosaka Y, Haissaguerre M, Aizawa Y
    Heart rhythm 11(12) 2261-2266 2014年12月 [査読有り]
  • Irbesartan-mediated AT1 receptor blockade attenuates hyposmotic-induced enhancement of I Ks current and prevents shortening of action potential duration in atrial myocytes.
    Wu J, Ding WG, Zhao J, Zang WJ, Matsuura H, Horie M
    Journal of the renin-angiotensin-aldosterone system : JRAAS 15(4) 341-347 2014年12月 [査読有り]
  • Author reply: To PMID 24394973.
    Ohno S, Horie M
    Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology 16(12) 1864-1865 2014年12月 [査読有り]
  • Long QT syndrome type 8: novel CACNA1C mutations causing QT prolongation and variant phenotypes.
    Fukuyama M, Wang Q, Kato K, Ohno S, Ding WG, Toyoda F, Itoh H, Kimura H, Makiyama T, Ito M, Matsuura H, Horie M
    Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology 16(12) 1828-1837 2014年12月 [査読有り]
  • Lipoprotein particle profiles compared with standard lipids in association with coronary artery calcification in the general Japanese population.
    Hisamatsu T, Fujiyoshi A, Miura K, Ohkubo T, Kadota A, Kadowaki S, Kadowaki T, Yamamoto T, Miyagawa N, Zaid M, Torii S, Takashima N, Murakami Y, Okamura T, Horie M, Ueshima H, SESSA Research Group.
    Atherosclerosis 236(2) 237-243 2014年10月 [査読有り]
  • High long-chain n-3 fatty acid intake attenuates the effect of high resting heart rate on cardiovascular mortality risk: A 24-year follow-up of Japanese general population.
    Hisamatsu T, Miura K, Ohkubo T, Yamamoto T, Fujiyoshi A, Miyagawa N, Kadota A, Takashima N, Okuda N, Yoshita K, Kita Y, Murakami Y, Nakamura Y, Okamura T, Horie M, Okayama A, Ueshima H, NIPPON DATA80 Research Group.
    J Cardiol 64(3) 218-224 2014年09月 [査読有り]
  • Comparison of long-term mortality after acute myocardial infarction treated by percutaneous coronary intervention in patients living alone versus not living alone at the time of hospitalization.
    Nakatsuma K, Shiomi H, Watanabe H, Morimoto T, Taniguchi T, Toyota T, Furukawa Y, Nakagawa Y, Horie M, Kimura T, CREDO-Kyoto AMI Investigators.
    The American journal of cardiology 114(4) 522-527 2014年08月 [査読有り]
  • Anticoagulant and antiplatelet therapy in patients with atrial fibrillation undergoing percutaneous coronary intervention.
    Goto K, Nakai K, Shizuta S, Morimoto T, Shiomi H, Natsuaki M, Yahata M, Ota C, Ono K, Makiyama T, Nakagawa Y, Furukawa Y, Kadota K, Takatsu Y, Tamura T, Takizawa A, Inada T, Doi O, Nohara R, Matsuda M, Takeda T, Kato M, Shirotani M, Eizawa H, Ishii K, Lee JD, Takahashi M, Horie M, Takahashi M, Miki S, Aoyama T, Suwa S, Hamasaki S, Ogawa H, Mitsudo K, Nobuyoshi M, Kita T, Kimura T, CREDO-Kyoto Registry Cohort-2 Investigators.
    The American journal of cardiology 114(1) 70-78 2014年07月 [査読有り]
  • Brugada syndrome in spinal and bulbar muscular atrophy.
    Araki A, Katsuno M, Suzuki K, Banno H, Suga N, Hashizume A, Mano T, Hijikata Y, Nakatsuji H, Watanabe H, Yamamoto M, Makiyama T, Ohno S, Fukuyama M, Morimoto S, Horie M, Sobue G
    Neurology 82(20) 1813-1821 2014年05月 [査読有り]
  • INVESTIGATION OF CLINICAL EFFICACY OF THROMBUS ASPIRATION ON 5-YEAR MORTALITY IN PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION UNDERGOING PCI
    Watanabe Hiroki, Kimura Takeshi, Morimoto Takeshi, Shiomi Hiroki, Taniguchi Tomohiko, Nakatsuma Kenji, Toyota Toshiaki, Nakagawa Yoshihisa, Furukawa Yutaka, Horie Minoru
    JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 63(12) A137 2014年04月 [査読有り]
  • Efficacy of bepridil to prevent ventricular fibrillation in severe form of early repolarization syndrome.
    Katsuumi G, Shimizu W, Watanabe H, Noda T, Nogami A, Ohkubo K, Makiyama T, Takehara N, Kawamura Y, Hosaka Y, Sato M, Fukae S, Chinushi M, Oda H, Okabe M, Kimura A, Maemura K, Watanabe I, Kamakura S, Horie M, Aizawa Y, Makita N, Minamino T
    International journal of cardiology 172(2) 519-522 2014年03月 [査読有り]
  • A KCNQ1 mutation contributes to the concealed type 1 long QT phenotype by limiting the Kv7.1 channel conformational changes associated with protein kinase A phosphorylation.
    Bartos DC, Giudicessi JR, Tester DJ, Ackerman MJ, Ohno S, Horie M, Gollob MH, Burgess DE, Delisle BP
    Heart rhythm 11(3) 459-468 2014年03月 [査読有り]
  • A molecular mechanism for adrenergic-induced long QT syndrome.
    Wu J, Naiki N, Ding WG, Ohno S, Kato K, Zang WJ, Delisle BP, Matsuura H, Horie M
    Journal of the American College of Cardiology 63(8) 819-827 2014年03月 [査読有り]
  • A Kir3.4 mutation causes Andersen-Tawil syndrome by an inhibitory effect on Kir2.1.
    Kokunai Y, Nakata T, Furuta M, Sakata S, Kimura H, Aiba T, Yoshinaga M, Osaki Y, Nakamori M, Itoh H, Sato T, Kubota T, Kadota K, Shindo K, Mochizuki H, Shimizu W, Horie M, Okamura Y, Ohno K, Takahashi MP
    Neurology 82(12) 1058-1064 2014年03月 [査読有り]
  • P-pulmonale and the development of atrial fibrillation.
    Hayashi H, Miyamoto A, Kawaguchi T, Naiki N, Xue JQ, Matsumoto T, Murakami Y, Horie M
    Circulation journal : official journal of the Japanese Circulation Society 78(2) 329-337 2014年 [査読有り]
  • Genetic and clinical advances in congenital long QT syndrome.
    Mizusawa Y, Horie M, Wilde AA
    Circulation journal : official journal of the Japanese Circulation Society 78(12) 2827-2833 2014年 [査読有り]
  • Long-term pharmacological therapy of Brugada syndrome: is J-wave attenuation a marker of drug efficacy?
    Hasegawa K, Ashihara T, Kimura H, Jo H, Itoh H, Yamamoto T, Aizawa Y, Horie M
    Internal medicine (Tokyo, Japan) 53(14) 1523-1526 2014年 [査読有り]
  • QT is longer in drug-free patients with schizophrenia compared with age-matched healthy subjects.
    Fujii K, Ozeki Y, Okayasu H, Takano Y, Shinozaki T, Hori H, Orui M, Horie M, Kunugi H, Shimoda K
    PloS one 9(6) e98555 2014年 [査読有り]
  • [Mechanisms for onset and maintenance of atrial fibrillation and its risk factors].
    Horie M
    Nihon rinsho. Japanese journal of clinical medicine 71(1) 29-35 2013年01月 [査読有り]
  • Pediatric Cohort with Short QT Syndrome
    Faulknier B., Kannankeril P., Makiyama T., Bleiz J., Hamilton R.M., Shimizu W., Young M.-L., Villafañe J., Gollob M.H., Atallah J., Wolpert C., Maury P., Watanabe H., Gebauer R., Anttonen O., Horie M.
    J Am Coll Cardiol 61(11) 1183-1191 2013年
  • LOX-1 ligands containing apolipoprotein B and carotid intima-media thickness in middle-aged community-dwelling US Caucasian and Japanese men.
    OKAMURA Tomonori, OKAMURA Tomonori, KADOWAKI Takashi, KADOTA Aya, MIURA Katsuyuki, FUJIYOSHI Akira, UESHIMA Hirotsugu, SEKIKAWA Akira, BARINAS‐MITCHELL Emma, MACKEY Rachel H., EVANS Rhobert W., KULLER Lewis H., SAWAMURA Tatsuya, FUJITA Yoshiko, KAKINO Akemi, EDMUNDOWICZ Daniel, HIGASHIYAMA Aya, NAKAMURA Yasuyuki, ABBOTT Robert D., MURAKAMI Yoshitaka, MIYAMATSU Naomi, MAEGAWA Hiroshi, MURATA Kiyoshi, HORIE Minoru, MITSUNAMI Kenichi, KASHIWAGI Atsunori
    Atherosclerosis 229(1) 240-245 2013年
  • Is More Aggressive Prevention of Coronary Artery Disease Required for Patients With Early Repolarization Syndrome?
    Hisamatsu T., Miura K., Ohkubo T., Ueshima H., Horie M.
    Circ J. 77(6) 1643 2013年
  • Time course and prognostic implications of QT interval in patients with coronary artery disease undergoing coronary bypass surgery.
    Kinoshita T, Asai T, Suzuki T, Matsubayashi K, Horie M
    J Cardiovasc Electrophysiol 23(6) 645-649 2012年06月 [査読有り]
  • The role of fibroblasts in complex fractionated electrograms during persistent/permanent atrial fibrillation implications for electrogram-based catheter ablation.
    Ashihara T, Haraguchi R, Nakazawa K, Namba T, Ikeda T, Nakazawa Y, Ozawa T, Ito M, Horie M, Trayanova NA
    Circulation Research 110(2) 275-284 2012年01月 [査読有り]
  • Clinical and electrocardiographic characteristics of patients with short QT interval in a large hospital-based population.
    Miyamoto A, Hayashi H, Yoshino T, Kawaguchi T, Taniguchi A, Itoh H, Sugimoto Y, Itoh M, Makiyama T, Xue JQ, Murakami Y, Horie M
    Heart Rhythm 9(1) 66-74 2012年01月 [査読有り]
  • Prognostic implications of progressive cardiac conduction disease.
    KAWAGUCHI Tamiro, HAYASHI Hideki, MIYAMOTO Akashi, YOSHINO Tomohide, TANIGUCHI Atsushi, NAIKI Nobu, SUGIMOTO Yoshihisa, ITO Makoto, XUE Joel Q., MURAKAMI Yoshitaka, HORIE Minoru
    Circ J. 77(1) 60-67 2012年
  • Seasonal and circadian distributions of cardiac events in genotyped patients with congenital long QT syndrome.
    TAKIGAWA Masateru, KAWAMURA Mihoko, NODA Takashi, YAMADA Yuko, MIYAMOTO Koji, OKAMURA Hideo, SATOMI Kazuhiro, AIBA Takeshi, KAMAKURA Shiro, SAKAGUCHI Tomoko, MIZUSAWA Yuka, ITOH Hideki, HORIE Minoru, SHIMIZU Wataru
    Circ J. 76(9) 2112-2118 2012年
  • Disease characterization using LQTS-specific induced pluripotent stem cells.
    EGASHIRA Toru, YUASA Shinsuke, SUZUKI Tomoyuki, SUZUKI Tomoyuki, AIZAWA Yoshiyasu, YAMAKAWA Hiroyuki, MATSUHASHI Tomohiro, OHNO Yohei, TOHYAMA Shugo, OKATA Shinichiro, SEKI Tomohisa, KURODA Yusuke, KURODA Yusuke, YAE Kojiro, HASHIMOTO Hisayuki, TANAKA Tomofumi, TANAKA Tomofumi, HATTORI Fumiyuki, HATTORI Fumiyuki, SATO Toshiaki, MIYOSHI Shunichiro, TAKATSUKI Seiji, MURATA Mitsushige, KUROKAWA Junko, FURUKAWA Tetsushi, MAKITA Naomasa, AIBA Takeshi, SHIMIZU Wataru, HORIE Minoru, KAMIYA Kaichiro, KODAMA Itsuo, OGAWA Satoshi, FUKUDA Keiichi
    Cardiovascular Research  95(4) 419-429 2012年
  • Clinical characteristics and risk of arrhythmia recurrences in patients with idiopathic ventricular fibrillation associated with early repolarization.
    WATANABE Hiroshi, HAYASHI Yuka, NAGAO Satomi, YAGIHARA Nobue, SATO Akinori, OKAMURA Kazuki, CHINUSHI Masaomi, AIZAWA Yoshifusa, NOGAMI Akihiko, OHKUBO Kimie, WATANABE Ichiro, KAWATA Hiro, KAMAKURA Shiro, SHIMIZU Wataru, ISHIKAWA Taisuke, KIMURA Akinori, MAKIYAMA Takeru, TAKEHARA Naofumi, KAWAMURA Yuichiro, HOSAKA Yukio, ODA Hirotaka, SATO Masahito, OKABE Masaaki, FUKAE Satoki, MAEMURA Koji, MAKITA Naomasa, HORIE Minoru
    Int J Cardiol. 159(3) 238-240 2012年
  • Comparison of long-term outcome after percutaneous coronary intervention versus coronary artery bypass grafting in patients with unprotected left main coronary artery disease (from the CREDO-Kyoto PCI/CABG Registry Cohort-2).
    SHIOMI Hiroki, TAZAKI Junichi, IMAI Masao, NATSUAKI Masahiro, SAIJO Sayaka, FUNAKOSHI Shunsuke, SHIZUTA Satoshi, KIMURA Takeshi, SAKATA Ryuzo, MORIMOTO Takeshi, HAYANO Mamoru, FURUKAWA Yutaka, EHARA Natsuhiko, KITA Toru, NAKAGAWA Yoshihisa, HANAZAWA Koji, YAMAJI Kyohei, IWABUCHI Masashi, NOBUYOSHI Masakiyo, HANYU Michiya, TADA Tomohisa, NAGAO Kazuya, KADOTA Kazushige, MITSUDO Kazuaki, ABE Mitsuru, OKABAYASHI Hitoshi, YAMAZAKI Fumio, SHIMAMOTO Mitsuomi, NISHIWAKI Noboru, IMOTO Yutaka, KOMIYA Tatsuhiko, HORIE Minoru, FUJIWARA Hisayoshi
    Am J Cardiol. 110(7) 924-932 2012年
  • Electrocardiographic characteristics and SCN5A mutations in idiopathic ventricular fibrillation associated with early repolarization.
    Circulation: Cardiovascular Genetics 5(3) 344-353 2012年
  • Chronic heart failure: progress in diagnosis and treatment. Topics: II. Progress in diagnosis: 2. Biomarker
    Nihon Naika Gakkai Zasshi 101(2) 345-53 2012年
  • Pharmacotherapeutic determinants for QTc interval prolongation in Japanese patients with mood disorder.
    Shimoda K., Okayasu H., Fujii K., Ozeki Y., Saeki Y., Takano Y., Horie M., Hori H., Kunugi H., Higuchi T.
    Pharmacopsychiatry 45(7) 279-283 2012年
  • Dynamicity of the J wave in idiopathic ventricular fibrillation with a special reference to pause-dependent augmentation of the J wave.
    Shinozaki T., Watanabe I., Fukuda K., Aizawa Y., Haissaguerre M., Joo K., Aizawa Y., Watanabe H., Sato A., Furushima H., Chinushi M., Kaneko Y., Horie M., Okubo K., Imaizumi T.
    Journal of American College of Cardiology  59(22) 1948-1953 2012年
  • Connexin 40 mutation associated with a malignant variant of familial progressive heart block type-1.
    Mochizuki N., Schott J.-J., Delmar M., Makita N., Sumitomo N., Seki A., Fukuhara S., Chkourko H., Shimizu W., Watanabe H., Hasdemir C., Bezzina C.R., Makiyama T., Mugishima H., Baron E., Baruteau A., Hagiwara N., Horie M., Probst V., Wilde A.A.M., Roden D.M., Le Marec H.
    Circulation Arrhythmia and Electrophysiology  5(1) 163-172 2012年
  • A novel gain-of-function KCNJ2 mutation associated with short QT syndrome impairs inward rectification of Kir2.1 currents.
    HATTORI Tetsuhisa, MAKIYAMA Takeru, AKAO Masaharu, EHARA Eiji, OHNO Seiko, IGUCHI Moritake, NISHIO Yukiko, SASAKI Kenichi, ITOH Hideki, YOKODE Masayuki, KITA Toru, HORIE Minoru, KIMURA Takeshi
    Cardiovascular Research  93(4) 666-673 2012年
  • Regional cooling facilitates termination of spiral-wave reentry through unpinning of rotors in rabbit hearts.
    Kamiya K., Jalife J., Kodama I., Yamazaki M., Ashihara T., Honjo H., Sakuma I., Harada M., Trayanova N., Nakazawa K., Kalifa J., Horie M.
    Heart Rhythm. 9(1) 107-114 2012年
  • KCNE3 T4A as the Genetic Basis of Brugada-Pattern Electrocardiogram
    NAKAJIMA Tadashi, WU Jie, WU Jie, KANEKO Yoshiaki, ASHIHARA Takashi, OHNO Seiko, IRIE Tadanobu, DING Wei-guang, MATSUURA Hiroshi, KURABAYASHI Masahiko, HORIE Minoru
    Circ J 76(12) 2763-2772 2012年
  • Regulatory mechanisms underlying the modulation of GIRK1/GIRK4 heteromeric channels by P2Y receptors
    WU Jie, WU Jie, WU Jie, DING Wei-Guang, MATSUURA Hiroshi, HORIE Minoru
    Pflugers Arch 463(4) 625-633 2012年
  • Identification and functional characterization of KCNQ1 mutations around the exon7-intron7 junction affecting the splicing process.
    Tsuji-Wakisaka K, Akao M, Ishii TM, Ashihara T, Makiyama T, Ohno S, Toyoda F, Dochi K, Matsuura H, Horie M
    BBA - Molecular Basis of Disease  1812(11) 1452-1459 2011年11月 [査読有り]
  • [Angina pectoris: classification and differential diagnosis].
    Yamamoto T, Horie M
    Nihon rinsho. Japanese journal of clinical medicine 69 Suppl 9 9-13 2011年11月 [査読有り]
  • Prognostic value of serial measurements of highly sensitive cardiac troponin I in stable outpatients with nonischemic chronic heart failure.
    Kawahara C, Tsutamoto T, Sakai H, Nishiyama K, Yamaji M, Fujii M, Yamamoto T, Horie M
    American Heart Journal 162(4) 639-645 2011年10月 [査読有り]
  • Angiotensin-converting enzyme inhibition and fibrinolytic balance.
    Matsumoto T, Horie M
    Hypertention Research 34(4) 448-449 2011年04月 [査読有り]
  • Remission of abnormal conduction and repolarization in the right ventricle after chemotherapy in patients with anterior mediastinal tumor.
    Miyamoto A, Hayashi H, Ito M, Horie M
    J Cardiovasc Electrophysiol.  22(3) 350-350 2011年03月 [査読有り]
  • Association between brachial-ankle pulse wave velocity and endothelium-dependent and -independent coronary vasomotor function.
    Yoshino T, Nakae I, Matsumoto T, Mitsunami K, Horie M
    Clin Exp Pharmacol Physiol.  38(1) 34-41 2011年01月 [査読有り]
  • Long-term safety and efficacy of sirolimus-eluting stents versus bare-metal stents in real world clinicalpractice in Japan.
    Tatami R., Suwa S., Takizawa A., Takatsu Y., Tanaka M., Aoyama T., Doi O., Hattori R., Takahashi M., Kato H., Kita T., Kimura T., Furukawa Y., Morimoto T., Kadota K., Nakagawa Y., Shizuta S., Iwabuchi M., Tada T., Shiomi H., Abe M., Mitsudo K., Kato Y., Tazaki J., Nobuyoshi M., Hayano M., Shirotani M., Tamura T., Matsuda M., Miki S., Ishii K., Takahashi M., Lee J.-D., Takeda T., Fujiwara H., Kambara H., Horie M., Tei C., Ogawa H., Nohara R.
    Cardiovascular Intervention and Therapeutics 26(3) 234-245 2011年
  • Carvedilol, a non-selective β-with α1-blocker is effective in long QT syndrome type2.
    KIMURA Hiromi, MIZUSAWA Yuka, ITOH Hideki, MIYAMOTO Akashi, KAWAMURA Mihoko, KAWAGUCHI Tamiro, NAIKI Nobu, OKA Yuko, OHNO Seiko, MAKIYAMA Takeru, ITO Makoto, HORIE Minoru
    Journal of Arrhythmia  27(4) 324-331 2011年
  • Effect of atorvastatin vs. rosuvastatin on cardiac sympathetic nerve activity in non-diabetic patients with dilated cardiomyopathy.
    TSUTAMOTO Takayoshi, TSUTAMOTO Takayoshi, SAKAI Hiroshi, IBE Kunihiro, YAMAJI Masayuki, KAWAHARA Chiho, NAKAE Ichiro, FUJII Masanori, YAMAMOTO Takashi, HORIE Minoru
    Circulation Journal  75(9) 2160-2166 2011年
  • Clinical characteristics and outcomes of Japanese women undergoing coronary revascularization therapy.
    FUNAKOSHI Shunsuke, FURUKAWA Yutaka, EHARA Natsuhiko, MORIMOTO Takeshi, KAJI Shuichiro, YAMAMURO Atsushi, KINOSHITA Makoto, KITAI Takeshi, KIM Kitae, TANI Tomoko, KOBORI Atsushi, NASU Michihiro, OKADA Yukikatsu, KITA Toru, KIMURA Takeshi, THE CREDO-KYOTO INVESTIGATORS
    Circulation Journal 75(6) 1358-1367 2011年
  • Electrocardiographic Characteristics and SCN5A Mutations in Idiopathic Ventricular Fibrillation Associated with Early Repolarization.
    Horie M., Aizawa Y., Shimizu W., Makita N., Kimura A., Maemura K., Watanabe I., Kamakura S., Watanabe H., Ohkubo K., Nogami A., Hayashi Y., Kawata H., Makiyama T., Ishikawa T., Yagihara N., Nagao S., Kawamura Y., Takehara N., Okamura K., Sato A., Sato M., Hosaka Y., Chinushi M., Fukae S., Okabe M., Oda H.
    Circulation: Arrhythmia and Electrophysiology 4(6) 874-881 2011年
  • Clinical characteristics and long-term prognosis of vasospastic angina patients who survived out-of-hospital cardiac arrest: multicenter registry study of the Japanese Coronary Spasm Association.
    SUEDA S, SATO T, OGAWA S, KUBO N, MOMOMURA S, OGAWA H, SHIMOKAWA H, TANABE Y, GOTO T, TAKAGI Y, YASUDA S, TSUNODA R, OGATA Y, SEKI A, SUMIYOSHI T, MATSUI M
    Circ Arrhythm Electrophysiol. 4(3) 295-302 2011年
  • Heritability of early repolarization: A population-based study.
    Hengstenberg C., Reinhard W., Debiec R., Kaess B.M., Stark K., Nelson C.P., MacFarlane P.W., Tobin M.D., Samani N.J., Tomaszewski M.
    Circulation Cardiovascular Genetics  4(2) 134-138 2011年
  • Phenotypic manifestations of mutations in genes encoding subunits of cardiac potassium channels.
    SHIMIZU Wataru, HORIE Minoru
    Circ Res. 109(1) 97-109 2011年
  • Relationship Between Biological Variation in B-Type Natriuretic Peptide and Plasma Renin Concentration in Stable Outpatients With Dilated Cardiomyopathy.
    Nishiyama K, Tsutamoto T, Kawahara C, Yamaji M, Sakai H, Yamamoto T, Fujii M, Horie M
    Circ J.  75(8) 1897-1904 2011年 [査読有り]
  • Risk determinants in individuals with a spontaneous type 1 Brugada ECG.
    Miyamoto A, Hayashi H, Makiyama T, Yoshino T, Mizusawa Y, Sugimoto Y, Ito M, Xue JQ, Murakami Y, Horie M
    Circulation Journal 75(4) 844-851 2011年 [査読有り]
  • Prognostic role of high-sensitivity cardiac troponin T in patients with nonischemic dilated cardiomyopathy.
    Kawahara C, Tsutamoto T, Nishiyama K, Yamaji M, Sakai H, Fujii M, Yamamoto T, Horie M
    Circ J 75(3) 656-661 2011年 [査読有り]
  • A Novel KCNJ2 Nonsense Mutation, S369X, Impedes Trafficking and Causes a Limited Form of Andersen-Tawil Syndrome.
    HORIE M, KIMURA T, TAKAHASHI Y, AKAO M, OHNO S, TSUJI K, HARUNA Y, MORIMOTO T, MAKIYAMA T, DOI T
    Circulation: Cardiovascular Genetics  4(3) 253-260 2011年
  • Novel KCNE5 variants are associated with Brugada syndrome and idiopathic ventricular fibrillation.
    HATTORI T, MIYAMOTO A, NAIKI N, HANCOX Jc, MATSUURA H, HORIE M, SHIZUTA S, DOI T, MAKIYAMA T, ITOH H, DING Wg, ZANKOV Dp, OHNO S
    Circulation Arrhythmia and Electrophysiology  4(3) 352-361 2011年
  • Reciprocal control of HERG stability by Hsp70 and Hsc70 with implication for restoration of LQT2 mutant stability.
    LI Peili, NINOMIYA Haruaki, KURATA Yasutaka, KATO Masaru, MIAKE Junichiro, YAMAMOTO Yasutaka, IGAWA Osamu, NAKAI Akira, HIGAKI Katsumi, TOYODA Futoshi, WU Jie, HORIE Minoru, MATSUURA Hiroshi, YOSHIDA Akio, SHIRAYOSHI Yasuaki, HIRAOKA Masayasu, HISATOME Ichiro
    Circ Res 108(4) 458-468 2011年
  • Lipocalin-Type Prostaglandin D Synthase Is Associated With Coronary Vasospasm and Vasomotor Reactivity in Response to Acetylcholine.
    Matsumoto T, Eguchi Y, Oda H, Yamane T, Tarutani Y, Ozawa T, Hayashi H, Nakae I, Horie M, Urade Y
    Circ J 75(4) 897-904 2011年 [査読有り]
  • Biological variation of brain natriuretic Peptide and cardiac events in stable outpatients with nonischemic chronic heart failure.
    Nishiyama K, Tsutamoto T, Yamaji M, Kawahara C, Fujii M, Yamamoto T, Horie M
    Circ J.  75(2) 341-347 2011年 [査読有り]
  • 循環器疾患における遺伝的背景と発症機序理解のための多面的アプローチ
    循環器内科 70 421-422 2011年
  • KCN]2変異を伴うAndersen-Tawil症候群の神経生理所見
    臨床神経生理学 39(1) 18-23 2011年
  • Heart rate-dependent variability of cardiac events in type 2 congenital long-QT syndrome.
    Nagaoka I, Shimizu W, Mizusawa Y, Sakaguchi T, Itoh H, Ohno S, Makiyama T, Yamagata K, Makimoto H, Miyamoto Y, Kamakura S, Horie M
    Europace  12(11) 1623-1629 2010年11月 [査読有り]
  • Atrioventricular block-induced torsades de Pointes with clinical and molecular backgrounds similar to congenital long QT syndrome.
    Oka Y, Itoh H, Ding WG, Shimizu W, Makiyama T, Ohno S, Nishio Y, Sakaguchi T, Miyamoto A, Kawamura M, Matsuura H, Horie M
    Circ J 74(12) 2562-2571 2010年11月 [査読有り]
  • Clinical features of myocardial triglyceride in different types of cardiomyopathy assessed by proton magnetic resonance spectroscopy: comparison with myocardial creatine.
    Nakae I, Mitsunami K, Yoshino T, Omura T, Tsutamoto T, Matsumoto T, Morikawa S, Inubushi T, Horie M
    J Card Fail  16(10) 812-822 2010年10月 [査読有り]
  • Long QT syndrome with compound mutations is associated with a more severe phenotype: a Japanese multicenter study.
    Itoh H, Shimizu W, Hayashi K, Yamagata K, Sakaguchi T, Ohno S, Makiyama T, Akao M, Ai T, Noda T, Miyazaki A, Miyamoto Y, Yamagishi M, Kamakura S, Horie M
    Heart Rhythm 7(10) 1411-1418 2010年10月 [査読有り]
  • Angiotensin-converting enzyme inhibition augments coronary release of tissue plasminogen activator in women but not in men.
    Matsumoto T, Takashima H, Nakae I, Yamane T, Hayashi H, Horie M, Shiga Plasminogen Activator in Coronary Circulation (SPAIC) Investigators.
    Hypertension  56(3) 364-368 2010年09月 [査読有り]
  • Relationship between exercise capacity and cardiac diastolic function assessed by time-volume curve from 16-frame gated myocardial perfusion SPECT.
    Yoshino T, Nakae I, Matsumoto T, Mitsunami K, Horie M
    Ann Nucl Med.  24(6) 469-476 2010年07月 [査読有り]
  • Characterization of the rapidly activating delayed rectifier potassium current, IKr, in HL-1 mouse atrial myocytes.
    Toyoda F, Ding WG, Zankov DP, Omatsu-Kanbe M, Isono T, Horie M, Matsuura H
    J Memb Biol 235(2) 73-87 2010年06月 [査読有り]
  • Pitavastatin reduces Lectin-Like oxidized low-density lipoprotein receptor-1 ligands in hypercholesterolemic humans.
    Matsumoto T, Fujita M, Sawamura T, Kakino A, Sato Y, Fujita Y, Matsuda H, Nakanishi M, Uchida K, Nakae I, Kanda H, Yoshida A, Miwa K, Hayashi H, Mitsunami K, Horie M
    Lipids 45(4) 329-335 2010年04月 [査読有り]
  • Comparison of the long-term effects of candesartan and olmesartan on plasma angiotensin II and left ventricular mass index in patients with hypertension.
    Tsutamoto T, Nishiyama K, Yamaji M, Kawahara C, Fujii M, Yamamoto T, Horie M
    Hypertens Res. 33(2) 118-122 2010年02月 [査読有り]
  • Prognostic role of highly sensitive cardiac troponin I in patients with systolic heart failure
    Tsutamoto T, Kawahara C, Nishiyama K, Yamaji M, Fujii M, Yamamoto T, Horie M
    Am Heart J 159(1) 63-67 2010年01月 [査読有り]
  • Prevalence and QT interval of early repolarization in a hospital-based population.
    HAYASHI Hideki, MIYAMOTO Akashi, ISHIDA Katsuya, YOSHINO Tomohide, SUGIMOTO Yoshihisa, ITO Makoto, HORIE Minoru
    Journal of Arrhythmia 26(2) 127-133 2010年
  • A novel SCN5A mutation associated with the linker between III and IV domains of Na(v)1.5 in a neonate with fatal long QT syndrome.
    YAMAMURA K., MUNEUCHI J., UIKE K., IKEDA K., INOUE H., TAKAHATA Y., HARA T., SHIOKAWA Y., YOSHIKANE Y., MAKIYAMA T., HORIE M.
    Int J Cardiol.  145(1) 61-64 2010年
  • Bi-directional ventricular tachycardia revised.
    Journal of Arrhythmia 26 3-4 2010年
  • A family of hereditary long QT syndrome caused by Q738X HERG mutation.
    YASUDA S., HIRAMATSU S.‐I., ODASHIRO K., MARUYAMA T., TSUJI K., HORIE M.
    Int J Cardiol.  144(1) 69-72 2010年
  • High prevalence of early repolarization in short QT syndrome.
    TANABE N, YAGIHARA N, KAMAKURA S, HORIE M, AIZAWA Y, SHIMIZU W, OKADA M, ITOH H, ODA H, WATANABE H, MAKIYAMA T, KOYAMA T, KANNANKERIL Pj, SETO S, OKAMURA K
    Heart Rhythm 7(5) 647-652 2010年
  • KCNE2 modulation of KV4.3 current and its potential role in fatal rhythm disorders.
    BRUGADA J, BRUGADA P, BRUGADA R, VATTA M, TOWBIN Ja, ANTZELEVITCH C, HORIE M, NADEMANEE K, MATSUURA H, KAMAKURA S, WU J, SHIMIZU W, DING Wg, OHNO S, TOYODA F, ITOH H, ZANG Wj, MIYAMOTO Y
    Heart Rhythm 7(2) 199-205 2010年
  • P-wave features with marked left atrial overload for predicting development of atrial fibrillation
    Heart Rhythm  7(3) 289-94 2010年
  • Clinical characteristics and genetic background of congenital long QT syndrome diagnosed in fetal, neonatal and infantile life. A nation-wide questionnaire survey in Japan.
    WAKI K, ARIMA M, TAKASUGI H, TANAKA Y, TAUCHI N, IKOMA M, INAMURA N, TAKAHASHI H, SHIMIZU W, HORIE M, GOTO H, MATSUNAGA T, HORIGOME H, NAGASHIMA M, SUMITOMO N, YOSHINAGA M, USHINOHAMA H, IWAMOTO M, SHIONO J, ICHIHASHI K, HASEGAWA S, YOSHIKAWA T
    Circ Arrhythm Electrophysiol.  3(1) 10-17 2010年
  • QTc prolongation and antipsychotic medications in a sample of 1017 patients with schizophrenia.
    OZEKI Y., FUJII K., OZEKI Y., KUNUGI H., KURIMOTO N., YAMADA N., OKAWA M., AOKI T., TAKAHASHI J., ISHIDA N., HORIE M.
    Progress in Neuro-Psychopharmacology & Biological Psychiatry  34(2) 401-405 2010年
  • 日本人の脳卒中、心筋梗塞、腎臓病に対するリスク因子の寄与度の違い:わが国の疫学研究から。
    Mebio 27(10) 30-44 2010年
  • カテコラミン誘発性多形性心室頻拍を疑う患者における遺伝子変異の検討-心筋リアノジン受容体について―Mutations of the cardiac ryanodine recepter gene in Catecholaminergic Polymorphic Ventricular Tachycardia
    川村美朋子, 長岡伊織, 道智賢市, 西尾由貴子, 伊藤英樹, 木村紘美, 宮本証, 水澤有香, 地藤優子, 石田勝也, 伊藤誠, 牧山武, 大野聖子, 住友直方, 小山耕太郎, 堀江稔
    心電図 30(4) 298-305 2010年
  • 遺伝性不整脈の診断と治療におけるiPS細胞利用の可能性。
    最新医学 139-145 2010年
  • 高血圧と不整脈:高血圧の治療によって不整脈発症の予防は可能か?
    Life Style Medicine 4 322-326 2010年
  • 日本人の心房細動における治療戦略の最新状況
    Trans BEAT 7 12-14 2010年
  • 高血圧治療薬としてのアンジオテンシンⅡ受容体拮抗薬とカルシウム拮抗薬の血管炎症および酸化ストレスに及ぼす影響。
    Prog.Med. 30(2) 469-472 2010年
  • 自動体外式除細動器による救命後に下肢切断を要したが心臓リハビリテーションにより回復した2症例。
    渋川武志, 林秀樹, 平岩康之, 木下妙子, 岩井宏冶, 前川昭次, 菊地克久, 今井晋二, 松本鉄也, 堀江稔
    心臓 42(6) 764-770 2010年
  • 運動中の心臓性突然死:成人の不整脈
    心電図 30(s-2) 13-24 2010年
  • デスモゾーム病としての不整脈源性右室心筋症-デスモゾーム分子遺伝子異常
    医学のあゆみ 232(5) 588-592 2010年
  • QTが長ければQT延長症候群か?
    medicina 47(1) 66-68 2010年
  • 遺伝子異常と不整脈
    臨床と研究 87(1) 98-101 2010年
  • Effect of simvastatin vs. rosuvastatin on adiponectin and haemoglobin A1c levels in patients with non-ischaemic chronic heart failure
    Tsutamoto T, Yamaji M, Kawahara C, Nishiyama K, Fujii M, Yamamoto T, Horie M
    Eur J Heart Fail 11(12) 1195-1201 2009年12月 [査読有り]
  • Dose-dependent prognostic effect of carvedilol in patients with chronic heart failure--special reference to transcardiac [corrected] gradient of norepinephrine.
    Nishiyama K, Tsutamoto T, Yamaji M, Kawahara C, Yamamoto T, Fujii M, Horie M
    Circulation journal : official journal of the Japanese Circulation Society 73(12) 2270-2275 2009年12月 [査読有り]
  • Serum cortisol as a useful predictor of cardiac events in patients with chronic heart failure -the impact of oxidative stress
    Yamaji M, Tsutamoto T, Kawahara C, Nishiyama K, Yamamoto T, Fujii M, Horie M
    Circulation Heart Fail  2(6) 608-615 2009年11月 [査読有り]
  • Aorto-Pulmonary Artery Dissection
    Itoh H, Yamamoto T, Sugihara H, Saotome T, Eguchi Y, Asai T, Horie M
    JACC  54(21) 1990 2009年11月 [査読有り]
  • Latent genetic backgrounds and molecular pathogenesis in drug-induced long QT syndrome.
    Itoh H, Sakaguchi T, Ding WG, Watanabe E, Watanabe I, Nishio Y, Makiyama T, Ohno S, Akao M, Higashi Y, Zenda N, Kubota T, Mori C, Okajima K, Haruna T, Miyamoto A, Kawamura M, Ishida K, Nagaoka I, Oka Y, Nakazawa Y, Yao T, Jo H, Sugimoto Y, Ashihara T, Hayashi H, Ito M, Imoto K, Matsuura H, Horie M
    Circulation 2(5) 511-523 2009年10月 [査読有り]
  • Effect of Simvastatin Versus Rosuvastatin on Adiponectin and Hemoglobin A1c Levels in Patients With Non-ischemic Chronic Heart Failure
    Yamaji Masayuki, Tsutamoto Takayoshi, Kawahara Chiho, Nishiyama Keizo, Yamamoto Takashi, Fujii Masanori, Horie Minoru
    JOURNAL OF CARDIAC FAILURE 15(7) S169 2009年09月 [査読有り]
  • Long-term effect of efonidipine therapy on plasma aldosterone and left ventricular mass index in patients with essential hypertension
    Tsutamoto T, Tanaka T, Nishiyama K, Yamaji M, Kawahara C, Fujii M, Yamamoto T, Horie M
    Hypertens Res 32(8) 670-674 2009年08月 [査読有り]
  • Relationship between renal function and serum cardiac troponin T in patients with chronic heart failure
    Tsutamoto T, Kawahara C, Yamaji M, Nishiyama K, Fujii M, Yamamoto T, Horie M
    Eur J Heart Fail  11(7) 653-658 2009年07月 [査読有り]
  • Adrenergic regulation of the rapid component of delayed rectifier K+ current: Implications for arrhythmogenesis in LQT2 patients.
    Zankov DP, Yoshida H, Tsuji K, Toyoda F, Ding WG, Matsuura H, Horie M
    Heart Rhythm 6(7) 1038-1046 2009年07月 [査読有り]
  • Endothelin-1 as a Predictor of Atrial Fibrillation Recurrence after Pulmonary Vein Isolation
    Nakazawa Y, Ashihara T, Tsutamoto T, Ito M, Horie M
    Heart Rhythm 6(6) 725-730 2009年06月 [査読有り]
  • Plasma NT-proBNP as a more reliable biomarker of endogenous cardiac natriuretic peptides Than BNP During Carperitide Infusion
    Nishiyama K, Tsutamoto T, Tanaka T, Fujii M, Yamamoto T, Yamaji M, Horie M
    Int Heart J 50(2) 183-190 2009年03月 [査読有り]
  • Dynamic change in ST-segment and spontaneous occurrence of ventricular fibrillation in brugada syndrome with a novel nonsense mutation in the SCN5AGene during long-term follow-up
    Kawamura M, Ozawa T, Yao T, Ashihara T, Sugimoto Y, Yagi T, Itoh H, Ito M, Makiyama T, Horie M
    Circ J 73(3) 584-588 2009年03月 [査読有り]
  • Dose-response effects of bepridil in patients with persistent atrial fibrillation monitored with transtelephonic electrocardiograms: a multicenter, randomized, placebo-controlled,double-blind study (J-BAF Study).
    YAMASHITA Takeshi, OGAWA Satoshi, SATO Toshiaki, AIZAWA Yoshifusa, ATARASHI Hirotsugu, FUJIKI Akira, INOUE Hiroshi, ITO Makoto, KATOH Takao, KOBAYASHI Youichi, KORETSUNE Yukihiro, KUMAGAI Koichiro, NIWANO Shinichi, OKAZAKI Osamu, OKUMURA Ken, SAKU Keijiro, TANABE Teruhisa, ORIGASA Hideki, THE J-BAF INVESTIGATORS
    Circ J.  73(6) 1020-1027 2009年
  • Novel KCNE3mutations interact with KCNQ1and cause long QT syndrome
    UEYAMA H, SHIMIZU W, MIYAMOTO Y, KAMAKURA S, MATSUURA H, KITA T, HORIE M, OBAYASHI K, HONDA T, OHNO S, TOYODA F, ZANKOV Dp, YOSHIDA H, MAKIYAMA T, TSUJI K
    Human Mutation  30(4) 557-563 2009年
  • A subclinical SCN5A mutation associated with drug-induced Brugada type ECG
    J Cardiovascular Electrophysiology 32(9) 1231-1236 2009年
  • Dose-dependent prognostic effect of carvedilol in patients with chronic heart failure--special reference to ranscardiac gradient of norepinephrine.
    NISHIYAMA Keizo, TSUTAMOTO Takayoshi, YAMAJI Masayuki, KAWAHARA Chiho, YAMAMOTO Takashi, FUJII Masanori, HORIE Minoru
    Circ J  73(12) 2270-2275 2009年
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    ITOH H, TSUJI K, SAKAGUCHI T, NAGAOKA L, OKA Y, NAKAZAWA Y, YAO T, JO H, ASHIHARA T, ITO M, HORIE M, IMOTO K
    Int J Cardiol 121(3) 239-248 2007年
  • Mechanistic basis for the pathogenesis of long QT syndrome associated with a common splicing mutation in KCNQ1 gene
    TSUJI K, AKAO M, ISHII Tm, OHNO S, MAKIYAMA T, TAKENAKA K, DOI T, HARUNA Y, YOSHIDA H, NAKASHIMA T, KITA T, HORIE M
    J Mol Cell Cardiol 42(3) 662-669 2007年
  • Stimulatory action of protein kinase Cε isoform on the slow component of delayed rectifier K+ current in guinea-pig atrial myocytes
    TODA H, DING Wg, YASUDA Y, TOYODA F, ITO M, MATSUURA H, HORIE M
    Br J Pharmacol 150(8) 1011-1021 2007年
  • Genotype-phenotype correlations of KCNJ2 mutations in Japanese patients with Andersen-Tawil syndrome
    Inoue T., Shimizu W., Tsuboi N., Murakami T., Ushinohama H., Yamanouchi H., Yoshinaga M., Nakamura Y., Aizawa Y., Horigome H., Kita T., Haruna Y., Makiyama T., Kobori A., Akao M., Yoshida H., Tsuji K., Doi T., Nishio Y., Ono S., Horie M.
    Hum Mutat 28(2) 208 2007年
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    The Journal of Physiological Scienses 57 S227 2007年
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    The Journal of Physiological Scienses 57 S227 2007年
  • Effect of artificial CO2 hot spring bathing on cholesterol crystal embolism after cardiac catheterization in a patient with normal coronary angiogram.
    Int Med J 6(1) C14 2007年
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    NAKAE I, MITSUNAMI K, MATSUO S, HORIE M
    Acta Radiol.  48(4) 436-443 2007年
  • Role of impaired sympathetic nerve function in enhancing coronary vasoconstriction in patients with hypertrophic cardiomyopathy
    Clin Exp Cardiol 12(17) 37-413A 2007年
  • N- and C-terminal KCNE1 mutations cause distinct phenotypes of long QT syndrome.
    OHNO S, ZANKOV Dp, YOSHIDA H, TSUJI K, MAKIYAMA T, ITOH H, AKAO M, HANCOX Jc, KITA T, HORIE M
    Heart Rhythm. 4(3) 332-340 2007年
  • A novel clinical indicator using Tc-99m sestamibi for evaluating cardiac mitochonddrial function in patients with cardiomyopathies.
    MATSUO S, NAKAE I, TSUTAMOTO T, OKAMOTO N, HORIE M
    J Nucl Cardiol  14(2) 215-220 2007年
  • 高血圧患者における早朝高血圧とメタボリックシンドロームとの関連
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    Long QT Syndrome 1(6) 2007年
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    心臓 39(11) 986-990 2007年
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    中澤優子, 芦原貴司, 稲垣菊代, 八尾武憲, 城日加里, 伊藤英樹, 杉本喜久, 伊藤誠, 堀江稔
    心電図 27(6) 657-659 2007年
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    QT間隔の診かた・考え方 131-132 2007年
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    循環器科 62(4) 393-399 2007年
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    心房細動 98-105 2007年
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    ICUとCCU 30(10) 669-677 2007年
  • 先天性QT延長症候群
    Long QT Syndrome 1-6 2007年
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    芦原貴司, 中澤優子, 八尾武憲, 城日加里, 伊藤英樹, 杉本喜久, 伊藤誠, 堀江稔
    心電図 27(4) 307-316 2007年
  • Ablation for AF:Techniques,Results and Risks
    AHA Highlights 2006 174-179 2007年
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    日本臨床 別冊 4 230-233 2007年
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    日本臨床 別冊 4 205-208 2007年
  • 軽度から中等度の本態性高血圧患者のAugmentation Index測定による評価ーアンジオテンシン受容体拮抗薬の効果ー
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  • 心筋リアノジン受容体の遺伝子変異(I4587V)を有したカテコラミン誘発性多形性心室頻拍の1成人症例
    道智賢市, 松本祐一, 長岡伊織, 伊藤誠, 芦原貴司, 伊藤英樹, 八尾武憲, 坂口知子, 中澤優子, 岡優子, 辻啓子, 堀江稔
    心電図 27(3) 246-252 2007年
  • 家族性心房細動を識る
    Heart View 11 84-86 2007年
  • 心臓イオンチャネル遺伝子の転写制御機構~エピジェネティックスと機能分化~
    心電図 27(S3) 15-28 2007年
  • Microvolt T Wave Alternansが反映する心室性不整脈発生基質:コンピュータシミュレーションによる基礎的検討
    心臓 39(Suppl.1) 14-19 2007年
  • 心房筋細胞におけるAT1受容体を介した緩徐活性型遅延整流性K+電流(IKs)の増大と活動電位の短縮-心房細動治療におけるAT1受容体遮断薬の有効性との関連-
    松浦博, ZANKOV Dimitar P., ZANKOV Dimitar P., 尾松万里子, 礒野高敬, 豊田太, DING Wei‐Guang, 堀江稔
    日本心電図学会誌 心電図 27(2) 145-153 2007年
  • Microvolt T wave alternansが反映する心室性不整脈発生基質ーコンピュータシミュレーションによる基礎的検討ー
    日本心臓財団.心臓 39(特別号1) 2007年
  • Brugada症候群と遺伝子病―Brugada症 候群とQT延長症候群など他の遺伝子病との関連について―
    Heart View 11(2) 54-61 2007年
  • The association between morning hypertension and metabolic syndrome hypertensive patients
    Tamaki Shinji, Nakamura Yasuyuki, Yoshino Tomohide, Matsumoto Yuichi, Tarutani Yasuhiro, Okabayashi Tabito, Kawashima Takeshi, Horie Minoru
    JOURNAL OF HYPERTENSION 24 271 2006年12月 [査読有り]
  • Regulation of blood pressure improves both coronary endothelial function and aortic stiffness in hypertensive patients.
    Matsumoto Tetsuya, Tarutani Yasuhiro, Yamane Tetsunobu, Takashima Hiroyuki, Matsuo Shinro, Horie Minoru
    JOURNAL OF HYPERTENSION 24 119 2006年12月 [査読有り]
  • Evaluation of cardiac resynchronization therapy in drug-resistant dilated-phase hypertrophic cardiomyopathy by means of Tc-99m sestamibi ECG-gated SPECT.
    Matsuo S, Sato Y, Nakae I, Masuda D, Matsumoto N, Horie M
    Ann Nucl Med 20(9) 643-647 2006年11月 [査読有り]
  • Blockade of T-type calcium channel suppressed the arrhythmogenicity in dominant negative NRSF transgenic mice
    Kinoshita Hideyuki, Kuwahara Kouichirou, Harada Masaki, Horie Minoru, Nakagawa Yasuaki, Nakanishi Michio, Usami Satoru, Fujiwara Masataka, Ueshima Kenji, Nakao Kazuwa
    JOURNAL OF CARDIAC FAILURE 12(8) S163 2006年10月 [査読有り]
  • Serum Level of Uric Acid, Partly Secreted From the Failing Heart, is a Prognostic Marker in Patients With Congestive Heart Failure
    Sakai H, Tsutamoto T, Tsutsui T, Tanaka T, Ishikawa C, Horie M
    Circ J 70(8) 1006-1011 2006年08月 [査読有り]
  • Prediction of mortality by high-sensitivity C-reactive protein and brain natriuretic Peptide in patients with dilated cardiomyopathy
    Ishikawa C, Tsutamoto T, Fujii M, Sakai H, Tanaka T, Horie M
    Circ J 70(7) 857-863 2006年07月 [査読有り]
  • Gender and Age Effects on Ventricular Repolarization Abnormality in Japanese General Carriers of a G643S Common Single Nucleotide Polymorphism for the KCNQ1 Gene.
    Ozawa T, Ito M, Tamaki S, Yao T, Ashihara T, Kita Y, Okamura T, Ueshima H, Horie M
    Circulation Journal 70(6) 645-650 2006年06月 [査読有り]
  • Impact of paraoxonase polymorphism (Q192R) on endothelial function in intact coronary circulation.
    Yamane T, Matsumoto T, Nakae I, Takashima H, Tarutani Y, Tamaki S, Horie M
    Hypertens Res 29(6) 417-422 2006年06月 [査読有り]
  • Angiotensin II potentiates the slow component of delayed rectifier K+ current via the AT1 receptor in guinea pig atrial myocytes
    Zankov DP, Omatsu-Kanbe M, Isono T, Toyoda F, Ding WG, Matsuura H, Horie M
    Circulation 113(10) 1278-1286 2006年03月 [査読有り]
  • Proteomic Analysis Reveals Significant Alternations of Cardiac Small Heat Shock Protein Expression in Congestive Heart Failure.
    Dohke T, Wada A, Isono T, Fujii M, Yamamoto T, Tsutamoto T, Horie M
    J Card Fail 12(1) 77-84 2006年02月 [査読有り]
  • Relationship between renal function and plasma brain natriuretic Peptide in patients with heart failure
    Tsutamoto T, Wada A, Sakai H, Ishikawa C, Tanaka T, Hayashi M, Fujii M, Yamamoto T, Dohke T, Ohnishi M, Takashima H, Kinoshita M, Horie M
    J Am Coll Cardiol 47(3) 582-586 2006年02月 [査読有り]
  • Impact of endothelial dysfunction on left ventricular remodeling after successful primary coronary angioplasty for acute myocardial infarction -Analysis by quantitative ECG-gated SPECT-.
    Matsuo S, Nakae I, Matsumoto T, Horie M
    Annals of Nuclear Medicine 20(1) 57-62 2006年01月 [査読有り]
  • Scintigraphic evaluatin of cardiac metabolism and sympathetic nerve function in alcoholic cardiomyopathy
    MATSUO Shinro, NAKAE Ichiro, MASUDA Daisuke, MATSUMOTO Tetsuya, HORIE Minoru
    Internal Medicine 45(7) 465-467 2006年
  • Mechanistic basis for the pathogenesis of long QT syndrome caused by a splicing mutation in KCNQ1 gene
    JMCC 2006年
  • The association between morning hypertension and metabolic syndrome in hypertensive patients
    TAMAKI Shinji, NAKAMURA Yasuyuki, YOSHINO Tomohide, MATSUMOTO Yuichi, TARUTANI Yasuhiro, OKABAYASHI Tabito, KAWASHIMA Takeshi, HORIE Minoru
    Hypertens Res 29(10) 783-788 2006年
  • Arrhythmogenesis in the short-QT syndrome associated with combined HERG channel gating defects: A Simulation Study
    ITOH Hideki, ITOH Hideki, HORIE Minoru, ITO Makoto, IMOTO Keiji
    Circulation Journal 70(4) 502-508 2006年
  • A novel mutation of plakophilin-2 associated with arrhythmogenic right ventricular cardiomyopathy
    NAGAOKA Iori, MATSUI Keiji, UEYAMA Takeshi, KANEMOTO Masashi, WU Jie, SHIMIZU Akihiko, MATSUZAKI Masunori, HORIE Minoru
    Circulation Journal 70(7) 933-935 2006年
  • Blockade of Angiotensin II type 1 receptor improves the arrhythmia morbidity in mice with left ventricular hypertrophy
    ZHANG Cuntai, ZHANG Cuntai, YASUNO Shinji, KUWAHARA Koichiro, ZANKOV Dimitar P., KOBORI Atsushi, MAKIYAMA Takeru, HORIE Minoru
    Circulation Journal 70(3) 335-341 2006年
  • Iodine-123 BMIPP scintigraphy in the evaluation of patients with heart failure.
    NAKAE I, MATSUO S, KOH T, MITSUNAMI K, HORIE M
    Acta Radiol. 47(8) 810-816 2006年
  • Relationship between the metabolic syndrome and TRP64ARG polymorphism of the beta3 adrenergic receptor gene in a general sample: The Shigaraki study.
    TAMAKI Shinji, NAKAMURA Yasuyuki, TABARA Yasuharu, OKAMURA Tomonori, KITA Yoshikuni, KADOWAKI Takashi, TSUJITA Yasuyuki, HORIE Minoru, MIKI Tetsuro, UESHIMA Hirotsugu
    Hypertens Res 29(11) 891-896 2006年
  • Nuclear Targeting of Akt Antagonizes Aspects of Cardiomyocyte Hypertrophy
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    Proc Natl Acad Sci U S A 103(32) 11946-11951 2006年
  • Molecular basis, natural history, and clinical outcome
    SCHWARTZ Pj, SPAZZOLINI C, CROTTI L, BATHEN J, AMLIE Jp, TIMOTHY K, SHKOLNIKOVA M, BERUL Ci, BITNER-GLINDZICZ M, TOIVONEN L, HORIE M, SCHULZE-BAHR E, DENJOY I
    Circulation 113(6) 783-790 2006年
  • JSH2004発表後の早朝高血圧の現状
    公立甲賀病院紀要 9 19-24 2006年
  • 不整脈の診断と治療:最近のトピックス
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    日本内科学会雑誌 95(3) 520-523 2006年
  • 不整脈の診断と治療:最近のトピックス
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    日本内科学会雑誌 95(3) 520-523 2006年
  • 不整脈研究の最新動向
    別冊・医学の歩み 217(6) 599-599 2006年
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  • 熱変性高速液体クロマトグラフィ法を用いたリアノジン受容体遺伝子変異のスクリーニング
    心臓 38(5) 533-535 2006年
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    Mebio 23(8) 116-126 2006年
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    医学のあゆみ 217(6) 599 2006年
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    Medical Practice 23(5) 823-824 2006年
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    循環器科 60(3) 229-234 2006年
  • 不整脈診断と治療:最近のトピックス
    日本内科学会雑誌 95(3) 108-111 2006年
  • Brugada症候群:基礎と臨床
    BIO Clinica 21(8) 736-742 2006年
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    心臓 38(9) 979-980 2006年
  • 座談会: New Evidence for EVENT REDUCTION in Hypertensive Patients.
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    医学のあゆみ 218 1361-1365 2006年
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    Int J Cardiovasc Imaging 21(4) 455-458 2005年08月 [査読有り]
  • Myocardial creatine concentration in various nonischemic heart diseases assessed by 1H magnetic resonance spectroscopy
    Nakae I, Mitsunami K, Matsuo S, Inubushi T, Morikawa S, Tsutamoto T, Koh T, Horie M
    Circ J 69(6) 711-716 2005年06月 [査読有り]
  • Refractory gradient is responsible for the increase in ventricular vulnerability under sodium channel blockade
    Yao T, Ashihara T, Ito M, Nakazawa K, Horie M
    Circ J 69(3) 345-353 2005年03月 [査読有り]
  • Open-state unblock characterizes acute inhibition of I potassium current by amiodarone in guinea pig ventricular myocytes.
    Zankov DP, Ding WG, Matsuura H, Horie M
    Journal of cardiovascular electrophysiology 16(3) 314-322 2005年03月 [査読有り]
  • High-risk for bradyarrhythmic complications in patients with Brugada syndrome caused by SCN5A gene mutations
    MAKIYAMA T, AKAO M, TSUJI K, DOI T, OHNO S, TAKENAKA K, KOBORI A, NINOMIYA T, YOSHIDA H, TAKANO M, MAKITA N, YANAGISAWA F, HIGASHI Y, TAKEYAMA Y, KITA T, HORIE M
    Journal of American College of Cardiology 46(11) 2100-2106 2005年
  • Inhibition of aldosterone and endothelin-1 by carperitide was attenuated more than one week Infusion in patients with congestive heart failure
    ISHIKAWA C, TSUTAMOTO T, WADA A, FUJII M, OHNO K, SAKAI H, YAMAMOTO T, HORIE M
    J Cardiovasc Pharmac 46(4) 513-518 2005年
  • In situ Ca2+ dynamics of Purkiinje fibers and its interconnection with subjacent ventricular myocytes
    HAMAMOTO T, TANAKA H, MANI H, TANABE T, FUJIWARA K, NAKAGAMI T, HORIE M, OYAMADA M, TAKAMATSU T
    J Mol Cell Cardiol 38(4) 561-569 2005年
  • Real-time confocal visualization of intracellular Ca dynamics of Purkinje fibers in Langendorff-perfused rat hearts
    Journal of Molecular and Cellular Cardiology 387 561-569 2005年
  • Clinical significance of plasma BNP measurement in patients with psychiatric disease.
    International Medical Journal 12 181-184 2005年
  • Cellular and ionic mechanism for drug-induced long QT syndrome and effectiveness of verapamil
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    J Am Coll Cardiol. 45(2) 300-307 2005年
  • Open-state unblock characterizes acute inhibition of IKs potassium current by amiodarone in guinea pig ventricular myocytes.
    ZANKOV Dp, DING Wg, MATSUURA H, HORIE M
    J Cardiovasc Electrophysiol 16(3) 314-322 2005年
  • Combined Analysis of Polymorphisms in Angiotensinogen and Adducin gene and Their Effects on Hypertension in a Japanese Sample: The Shigaraki Study
    TAMAKI Shinji, NAKAMURA Yasuyuki, TABARA Yasuharu, OKUMURA Tomonori, KITA Yoshikuni, KADOWAKI Takashi, TSUJITA Yasuyuki, HORIE Minoru, MIKI Tetsuro, UESHIMA Hirotsugu
    Hypetens Res 28(8) 645-650 2005年
  • ECG features in Andersen-Tawil syndrome patients with KCNJ2 mutations - Characteristic T-U wave patterns predict the genotype
    ZHANG L, BENSON Dw, TRISTANI-FIROUZI M, PTACEK Lj, TAWIL R, SCHWARTZ Pj, GEORGE Al, HORIE M, ANDELFINGER G, SNOW Gl, FU Yh, ACKERMAN Mj, VINCENT Gm
    Circulation 111(21) 2720-2726 2005年
  • Regulation of the muscarinic K channel by extracellular ATP through membrane phosphatidylinositol 4,5-biphsopahte in guinea-pig
    YASUDA Y, MATSUURA H, ITO M, MATSUMOTO T, DING Wg, HORIE M
    British Journal of Pharmacology 145(2) 156-165 2005年
  • Detection of calf muscle alterations in patients with chronic heart failure by 31P magnetic resonance spectroscopy: Impaired ada
    Exp Clin Cardiol 10 4-8 2005年
  • Effect of statin therapy on arterial stiffness in patients with hyperlipidemia : Shiga pravastatin atherosclerosis study (SHIPAS
    Journal of Applied Research 5 397-401 2005年
  • Double SCN5A mutation underlyng asymptomatic Brugada syndrome
    YOKOI H, MAKITA N, SASAKI K, TAKAGI Y, OKUMURA Y, NISHINO T, MAKIYAMA T, KITABATAKE A, HORIE M, WATANABE I, TSUTSUI H
    Heart Rhythm 2(3) 285-292 2005年
  • Brachial artery flow-mediated vasodilation is correlated with coronary vasomotor and fibrinolytic responses induced by bradykini
    TARUTANI Yasuhiro, MATSUMOTO Tetsuya, TAKASHIMA Hiroyuki, YAMANE Tetsunobu, HORIE Minoru
    Hypertension Res 28(1) 59-66 2005年
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    Therapeutic Research 26(7) 1487-1491 2005年
  • 不整脈の背景 ? イオンチャネルと活動電位
    Heart View 9(12) 12-18 2005年
  • 遺伝性QT延長・短縮症候群
    最新医学 60(10) 38-44 2005年
  • 体液因子による心不全の評価
    蔦本尚慶, 堀江稔
    日本内科学会雑誌 94(2) 221-227 2005年
  • 右側中中隔と冠状静脈洞入口部下縁とに複数心房付着端を有したWPW症候群に対しカテーテル・アブレーションを施行した1例
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    内科 96 989-998 2005年
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    Life Science 73(24) 3083-3094 2003年10月 [査読有り]
  • Verapamil, a Ca2+ Entry Blocker, Targets the Pore-Forming Subunit of Cardiac Type KATP Channel(Kir6.2).
    NINOMIYA T, TAKANO M, HARUNA T, KONO Y, HORIE M
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    Cardiovascular Research 34(1) 69-72 1997年
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  • fuzzy space ATPは虚血再灌流不整脈の発生に関与するか?-ATP感受性カリウム・チャネルとトランスポータ蛋白の機能的協関-
    堀江稔, 綿貫正人, 土屋邦彦, 高橋綾子, 篠山重威
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  • Block of pancreatic ATP-sensitive K+ channels and insulinotrophic action by antiarrhythmic agent cibenzoline.
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  • Cloning and functional characterization of a novel ATP-sensitive potassium channel ubiquitously expressed in rat tissues, inclu
    INAGAKI N, TSUURA Y, NAMBA N, MASUDA K, GONOI T, HORIE M, SEINO Y, MIZUTA M, SEINO S
    Journal of Biological Chemistry 270(11) 5691-5694 1995年
  • A fast transient outward current in cultured cells from human pulmonary artery smooth muscle.
    American Journal of Physiology 268 H2358-H2365 1995年
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  • ETA receptors mediate inhibition of the cardiac PKA-dependent Cl-current via a pertussis toxin-sensitive mechanism.
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  • Involvement of pertussis toxin-sensitive G-proteins in the mechanism of postvagal potentiation of cardiac calcium and chloride c
    Heart and Vessels 9 58-60 1995年
  • 細胞内流とgiant excised-patch法
    日本生理学雑誌 57(1) 15-23 1995年
  • Function of CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) chloride channels expressed in mammalian cardiac myocytes
    Japanese Heart Journal 35 S-1-63-S-1-68 1994年
  • Nitric oxide opens ATP-sensitive K+ channels through suppression of phosphofructokinase activity and inhibits glucose-induced in
    Journal of General Physiology 79 1078-1098 1994年
  • Reduced sensitivity of dihydroxyacetone on ATP-sensitive K+ channels of pancreatic ?
    Diabetologia 37 1082-1087 1994年
  • Regulation of CFTR channel gating.
    Japanese Journal of Physiology 44 S183-S192 1994年
  • Additional similarity of cardiac cAMP-activated Cl- channels to CFTR Cl- channels.
    Japanese Journal of Physiology 44 S215-218 1994年
  • The effects of endothelin-1 on the PKA-dependent Cl- current in the heart.
    Japanese Journal of Physiology 44 S227-S230 1994年
  • Inhibitory pathway of cardiac PKA-dependent Cl- conductance via pertussis toxin-sensitive G proteins.
    Japanese Journal of Physiology 44 S219-S226 1994年
  • Increased calcium-channel currents of pancreatic ?
    Metabolism 43 1395-1400 1994年
  • Inhibition of the cardiac protein kinase A-dependent chloride conductance by endothelin-1.
    JAMES A F, XIE L‐H, FUJITANI Y, HAYASHI S, HORIE M
    Nature 370(6487) 297-300 1994年
  • Cardiac chloride channels: incremental regulation by phosphorylation/ dephosphorylation. in Molecular Basis of Ion Channels and
    GADSBY D C, HWANG T‐C, HORIE M, NAGEL G, NAIRN A C
    Annals of The New York Academy of Sciences 707 259-274 1993年
  • Glucose sensitivity of ATP-sensitive K+ channels is impaired in ?
    Diabetes 42 1446-1453 1993年
  • Disopyramide blocks pancreatic ATP-sensitive K+ channels and enhances insulin release.
    American Journal of Physiology 265 C337-C342 1993年
  • Functionally distinct phospho-forms underlie incremental activation of protein kinase-regulated Cl- conductance in mammalian hea
    Journal of General Physiology 101 629-650 1993年
  • On the mechanism of minoxidil sulfate-induced shortening of action potential durations in guinea pig ventricular myocytes.
    Journal of Pharmacology and Experimental Therapeutics 256 1527-1533 1993年
  • Activation of Ca- permeable cation channels by myocarditis-associated antibody in guinea pig ventricular myocytes.
    Journal of Clinical Investigation 91 1231-1234 1993年
  • 自律神経と心筋イオンチャネル
    心電図 (Jpn J Electrocardiology)  13 S3-S20 1993年
  • 哺乳類単離心筋細胞膜電流と細胞内カルシウムの同時測定:カフェインの作用について
    財団法人 横山臨床薬理研究助成基金研究業績輯 1 94-100 1993年
  • On the mechanism of b-adrenergic activation of cardiac outward currents.
    Japanese Circulation Journal 56 S1344-1348 1992年
  • Comparative studies of ATP sensitive potassium channels in heart and pancreatic ?
    Cardiovascular Research 26 1087-1094 1992年
  • Role of GTP-binding proteins in the regulation of mammalian cardiac chloride conductance.
    Journal of General Physiology 99 465-489 1992年
  • Impaired glucose sensitivity of ATP-sensitive K+ channels in pancreatic B cells in streptozotocin-induced NIDDM rats.
    Diabetes 41 861-865 1992年
  • Pipette GTP is essential for receptor-mediated regulation of Cl- current in dialysed myocytes from guinea-pig ventricle.
    Journal of Physiology 455 235-246 1992年
  • 心筋細胞とマグネシウム
    CURRENT CONCEPTS IN MAGNESIUM METABOLISM 5 9-11 1992年
  • β-アドレナリン受容体を介する心筋細胞膜電流活性化の細胞内分子機構
    Japanese Circulation Journal 56(5) 1344-1348 1992年
  • Nicorandil reduces the basal level of cytosolic free calcium in single guinea pig ventricular myocytes.
    HORIE M, SUZUKI H, HAYASHI S, ZANG W‐J, KOMORI M, OKADA Y, FUJITA J, KAWAI C
    Cell Structure and Function 16(6) 433-440 1991年
  • Kinetic analyses of creatine kinase release patterns in patients with acute myocardial infarction undergoing emergency coronary
    HORIE M, MIYAZAKI S, NONOGI H, TAKIZAWA A, NAGAO M, NISHIDA S, KUBOTA J, KAWAI C
    Japanese Circulation Journal 54(5) 478-486 1990年
  • Two types of delayed rectifying K+ channels in atrial cells of guinea pig heart.
    HORIE M, HAYASHI S, KAWAI C
    Japanese Journal Physiology 40(4) 479-490 1990年
  • Atrial natriuretic peptide reduces the basal level of cytosolic free Ca2+ in guinea pig cardiac myocytes.
    TEI M, HORIE M, MAKITA T, SUZUKI H, HAZAMA A, OKADA Y, KAWAI C
    Biochemical Biophysical Research Communication 167(2) 413-418 1990年
  • Fura-2 螢光比画像解析による単離心筋細胞内Ca2+測定-各種Ca拮抗薬の効果-
    薬理と治療 18(2) 91-102 1990年
  • Dual effects of intracellular magnesium on muscarinic potassium channel current in single guinea-pig atrial cells.
    Journal of Physiology (Lond.) 408 313-332 1989年
  • Electrophysiological effects of melperone on isolated rabbit heart muscles.
    British Journal of Pharmacology 94 1063-1068 1988年
  • 心筋カリウムチャネル内向き整流特性と細胞内マグネシウム
    心臓 20(5) 635-641 1988年
  • Rectification of muscarinic K+ current by magnesium ion in guinea pig atrial cells.
    American Journal of Physiology 253 H210-H214 1987年
  • Voltage-dependent magnesium block of adensosine-triphosphate-sensitive potassium channel in guinea-pig ventricular cells.
    Journal of Physiology (Lond.) 387 251-272 1987年
  • Pathogenesis of angina pectoris in patients with one-vessel disease: possible role of dynamic coronary obstruction.
    American Heart Journal 112 263-272 1986年
  • A new approach for the enzymatic estimation of infarct size: serum creatine kinase and time to peak creatine kinase activity.
    American Journal of Cardiology 57 76-81 1986年
  • Role of coronary spasm in different anginal syndromes.
    Acta Medica Scandinavica 694 83-94 1985年
  • :心筋梗塞急性期における責任冠動脈のspontaneous reperfusion: 血中creatine phosphokinase遊出胴体と慢性期心機能による検討
    日本内科学会誌 9 41-45 1985年
  • Variant angina induced by alcohol ingestion.
    American Heart Journal 107 25-27 1984年
  • The effects of reperfusion of infarct-related coronary artery on serum creatine phosphokinase and left ventricular function.
    HORIE M, YASUE H, OMOTE S, TAKIZAWA A, NAGAO M, NISHIDA S, KUBOTA J
    Japanese Circulation Journal 48(6) 539-545 1984年
  • 冠動脈スパズム診断の進歩
    クリニカ 11 57-61 1984年
  • 心筋虚血発作における冠攣縮の関与
    臨床科学 20(1) 15-21 1984年
  • 初回心筋梗塞急性期の側副血行について  
    最新医学 39 2203-2205 1984年
  • 心筋梗塞急性期冠動脈造影法施行例50名における急性期creatine phosphokinaseの検討
    心臓 16 799-805 1984年
  • 急性心筋梗塞における冠動脈内血栓溶解療法の左室壁運動に対する効果
    最新医学 39 1071-1073 1984年
  • Coronary arteriographic findings during early hours of acute myocardial infarction: response to intracoronary infusion of nitrat
    Angiology 34 553-560 1983年
  • 冠動脈造影法-器質的狭窄と冠攣縮
    Pharma Medica  1 65-72 1983年
  • 心筋梗塞急性期の冠動脈造影所見と血栓溶解療法
    最新医学 38 812-813 1983年
  • 肥大型心筋症に対する塩酸ジルチアゼムの効果
    薬理と治療  30 235-240 1982年
  • 心筋梗塞急性期の冠動脈造影所見
    呼吸と循環  30 83-90 1982年
  • Diltiazem-induced decrease of exercise-elevated pulmonary arterial diastolic pressure in hypertrophic cardiomyopathy patients.
    American Heart Journal 102 789-790 1981年
  • Comparison of coronary arteriographic findings during angina pectoris associated with ST segment elevation or depression.
    American Journal of Cardiology 47 539-546 1981年

書籍等出版物

  • イオンチャネル病のすべて
    堀江 稔
    医歯薬出版 2014年
  • ブルガダ症候群
    医学書院 2011年
  • 抗不整脈薬の使い方 1
    日本循環器学会, 堀江 稔, 新 博次
    医学映像教育センター 2010年
  • 厚生労働科学研究費補助金難治性疾患克服研究事業家族性突然死症候群の遺伝的背景の解明に関する研究研究報告書
    堀江 稔
    [堀江稔] 2010年
  • 今日の治療方針 私はこう治療している 2010年度版 心房細動
    医学書院 2010年
  • ARB/ACE-1 による心房細動抑止効果 Annual Review 循環器 2010
    中外医学社 2010年
  • 脚ブロック
    南江堂 2010年
  • QT延長症候群
    循環器疾患のサイエンス 2010年
  • 肥大型心筋症 β遮断薬 115.アテノール
    中外医学社 2010年
  • Ⅱ 疾患編 4循環器疾患 QT延長症候群 今日の診断指針 第6版
    医学書院 2010年
  • 3.β遮断薬、α遮断薬、αβ遮断薬
    文光社 2010年
  • QT短縮症候群における突然死
    医学書院 2010年
  • 今日の治療指針 私はこう治療している2010年度版 心房細動
    医学書院 2010年
  • Annual Review 循環器 2010:ARB/ACE-Iによる心房細動抑止効果。
    中外医学社  2010年
  • 脚ブロック 循環器疾患最新の治療2010-2011
    南江堂 2010年
  • 重篤副作用疾患別対応マニュアル:心室頻拍
    厚生労働省 2009年
  • 最新医学別冊 新しい診断と治療のABC15 循環器2 心房細動(改訂第2版)
    株式会社 最新医学社 2009年
  • 慢性腎臓病患者における心機能の血清学的診断
    羊土社 2008年
  • 心不全
    レジデントのための栄養管理基本マニュアル 2008年
  • 循環器病疾患最新の治療
    南江堂 2008年
  • 別冊「医学のあゆみ」不整脈研究の最新動向
    堀江稔
    単著
    医歯薬出版 2007年04月
  • 不整脈研究の最新動向
    堀江 稔
    医歯薬出版 2007年
  • 致死性不整脈の遺伝子診断 Annual Review 循環器 2007
    中外医学社 2007年
  • BNP濃度測定の意義?重症度、病態把握、治療効果判定
    心不全(上) 2007年
  • Annual Review 循環器 2006 不整脈領域におけるチャネル病
    中外医学社 2006年
  • 循環器疾患最新の治療2006-2007 心不全における不整脈の治療
    南江堂 2006年
  • 不整脈と原因遺伝子
    日本内科学会 2006年
  • 心不全における神経体液性因子. 新目で見る循環器病シリーズ 9 心不全-診断・治療・管理
    株式会社メジカルビュー社 2006年
  • Brugada症候群と遺伝子異常 臨床心臓病学
    文光堂 2006年
  • 頻脈性不整脈を診る・治す QT延長症候群 病態・分類・検査. 新・心臓病診療プラクティス 7 心電図で診る・治す
    文光堂 2006年
  • BNPと心不全―エビデンスを中心に―. 新BNPと日常臨床―心機能異常の早期発見のために―
    南江堂 2005年
  • 不整脈2003 Medical Topics Series : QT延長症候群と遺伝子異常
    メディカルレビュー社 2003年
  • 不整脈診療ガイダンス : QT延長症候群の分類と遺伝子異常について最近の知見を教えてください
    メジカルビュー社 2003年
  • 新パッチクランプ実験技術法 : 細胞内灌流法
    吉岡書店 2003年
  • 最新医学 別冊 ABC15 心房細胞
    最新医学社 2003年
  • 今月の治療 VOL.11増刊 循環器疾患治療スタンダード2004-2005 : 不整脈治療薬の催不整脈作用
    総合医学社 2003年
  • ナースのための循環器科 : 心疾患を知る-不整脈
    メディカ出版 2003年
  • QT延長症候群 : 循環器疾患最新の治療2002-2003
    南江堂 2002年

MISC

  • BNP異常高値の原因がmacro‐proBNP血症であった症例
    中川靖章, 錦見俊雄, 錦見俊雄, 酒井宏, 大野聖子, 木下秀之, 稲住英明, 森内健史, 柳澤洋, 桑原宏一郎, 堀江稔, 木村剛
    日本内分泌学会雑誌 94(1) 347 2018年04月
  • 非発作性心房細動における興奮波ダイナミクスは構造的リモデリング指標よりも年齢によって規定される―ExTRa Mapping Project―
    坂田憲祐, 小澤友哉, 奥山雄介, 原口亮, 稲田慎, 中沢一雄, 土谷健, 堀江稔, 芦原貴司
    心電図 38(Supplement 1) 68-1 2018年03月
  • 『ベラパミル感受性特発性心室頻拍』
    伊藤誠, 小澤友哉, 芦原貴司, 杉本喜久, 堀江稔
    滋賀医学 40 59‐60 2018年03月
  • 意識消失発作を主訴とした成人型筋緊張性ジストロフィーの1例
    冨岡大資, 小澤友哉, 大野聖子, 伊藤英樹, 芦原貴司, 山本孝, 堀江稔
    滋賀医学 40 49 2018年03月
  • 長期持続性心房細動に対するExTRa Mappingガイド下非受動興奮領域アブレーションの有用性―ExTRa Mapping Project―
    芦原貴司, 坂田憲祐, 奥村雄介, 小澤友哉, 原口亮, 稲田慎, 中沢一雄, 土谷健, 堀江稔
    心電図 38(Supplement 1) 59-1 2018年03月
  • 『循環器疾患と臨床遺伝学』
    堀江稔
    滋賀医学 40 95 2018年03月
  • Brugada症候群における飲酒後失神に寄与するscore systemの構築
    呉き, 平大樹, 林秀樹, 園田佳子, 大野聖子, 牧山武, 寺田智祐, 堀江稔
    心電図 38(Supplement 1) 14-1 2018年03月
  • 遺伝性不整脈診断に関連した最新の動向とリスク評価について
    堀江稔
    心電図 38(Supplement 1) 8-1 2018年03月
  • RYR2遺伝子変異が判明した乳児期発症QT延長症候群症例の臨床経過
    星合美奈子, 星合美奈子, 喜瀬広亮, 河野洋介, 吉沢雅史, 小泉敬一, 廣瀬紗也子, 大野聖子, 堀江稔, 杉田完爾, 戸田孝子
    日本小児科学会雑誌 122(2) 246-246 2018年02月
  • 脊椎麻酔併用骨盤位外回転術(ECV)の有用性とECV関連合併症の検討
    石橋弘樹, 吉永洋輔, 角倉仁, 大塚由花, 岩橋秀樹, 松浦寛子, 澁谷剛志, 堀江稔, 古谷健一, 村上充剛
    日本産科婦人科学会雑誌 70(2) 981 2018年02月
  • 脊椎クモ膜下硬膜外併用麻酔で吸引娩出術を施行した6例
    岩橋秀樹, 吉永洋輔, 角倉仁, 大塚由花, 石橋弘樹, 澁谷剛志, 松浦寛子, 堀江稔, 村上充剛
    日本産科婦人科学会雑誌 70(2) 885 2018年02月
  • 遺伝子解析検査が薬物選択に有効であった,QT延長を呈する心室細動の1例
    坂部茂俊, 海野航平, 伊藤弘将, 後藤至, 刀根克之, 高村武志, 堀口昌秀, 前野健一, 泉大介, 世古哲哉, 笠井篤信, 大野聖子, 堀江稔
    心臓 49(Suppl.2) 218-218 2017年11月
  • 心房細動に対する基質アブレーションの可能性
    芦原貴司, 坂田憲祐, 堀江稔
    臨床医のための循環器診療(27) 56‐59-59 2017年11月
  • 慢性心房細動アブレーションの新たな治療戦略に向けたインシリコの応用
    芦原貴司, 芦原貴司, 坂田憲祐, 奥山雄介, 小澤友哉, 土谷健, 原口亮, 稲田慎, 中沢一雄, 堀江稔, 杉本喜久, 永田啓
    医療情報学連合大会プログラム・抄録集 37th 364 2017年11月
  • A SCN5A Variant Associated with Drug Induced Brugada Type ECG(和訳中)
    藍 智彦, 三井田 孝, 堀江 稔
    臨床病理 65(補冊) 268-268 2017年10月
  • ラミノパチー患者に対する両室再同期療法は心不全予後を改善させるか?
    中島 健三郎, 相庭 武司, 西内 英, 牧山 武, 尾上 健児, 鎌倉 令, 和田 暢, 石橋 耕平, 岡村 英夫, 大野 聖子, 宮本 恵宏, 斎藤 能彦, 堀江 稔, 清水 渉, 草野 研吾
    日本心臓病学会学術集会抄録 65回 O-030 2017年09月
  • 著明な左室収縮能低下と徐脈を認めplakophilin 2遺伝子変異による不整脈原性右室心筋症と診断した1例
    高橋 友香里, 久保 亨, 越智 友梨, 高橋 有紗, 宮川 和也, 野口 達哉, 弘田 隆省, 山崎 直仁, 堀江 稔, 北岡 裕章
    日本心臓病学会学術集会抄録 65回 P-068 2017年09月
  • Timothy症候群亜型におけるCACNA1C新規遺伝子変異の同定と電気生理学的検討
    小澤 淳一, 大野 聖子, 鈴木 博, 齋藤 昭彦, 松浦 博, 堀江 稔
    日本小児科学会雑誌 121(8) 1426-1427 2017年08月
  • Timothy症候群亜型におけるCACNA1C新規遺伝子変異の同定と電気生理学的検討
    小澤淳一, 小澤淳一, 小澤淳一, 大野聖子, 大野聖子, 鈴木博, 齋藤昭彦, 松浦博, 堀江稔
    日本小児科学会雑誌 121(8) 1426‐1427-1427 2017年08月
  • 一般健常男性における喫煙習慣・禁煙期間と潜在性動脈硬化指標との関連:滋賀動脈硬化疫学研究SESSA
    久松隆史, 久松隆史, 久松隆史, 三浦克之, 有馬久富, 門田文, 門脇紗也佳, 鳥居さゆ希, 鈴木仙太朗, 宮川尚子, 佐藤敦, 藤吉朗, 大久保孝義, アボット ロバート, 関川暁, 堀江稔, 上島弘嗣
    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web) 49th 112 (WEB ONLY)-112 2017年06月
  • QT延長を伴うカテコラミン誘発多形性心室頻拍(CPVT)の3例
    西藤陽, 二宮由美子, 田中裕治, 塗木徳人, 大野聖子, 堀江稔, 吉永正夫
    日本小児科学会雑誌 121(7) 1267‐1268-1268 2017年07月
  • 心房細動患者におけるアピキサバンの母集団薬物動態解析
    山根拓也, 上島智, 平大樹, 木村悠馬, 藤井亮, 冨塚知歩, 田淵陽平, 伊藤英樹, 大野聖子, 小澤友哉, 堀江稔, 寺田智祐, 桂敏也
    医療薬学フォーラム講演要旨集 25th 233 2017年06月
  • 一般健常男性における喫煙習慣・禁煙期間と潜在性動脈硬化指標との関連 滋賀動脈硬化疫学研究SESSA
    久松 隆史, 三浦 克之, 有馬 久富, 門田 文, 門脇 紗也佳, 鳥居 さゆ希, 鈴木 仙太朗, 宮川 尚子, 佐藤 敦, 藤吉 朗, 大久保 孝義, アボット・ロバート, 関川 暁, 堀江 稔, 上島 弘嗣
    日本動脈硬化学会総会プログラム・抄録集 49回 112-112 2017年06月
  • 心房細動患者におけるアピキサバンの血中濃度に及ぼす薬物動態関連遺伝子多型の影響
    上島智, 平大樹, 堀江稔, 寺田智祐, 桂敏也
    臨床薬理の進歩(38) 104‐112-112 2017年06月
    アピキサバンの錠剤を内服した成人心房細動(AF)患者44例(男性36例、女性8例、38.3〜80.1歳)を対象とした。データ数は70点で、アピキサバンの血中濃度の中央値は137ng/mLであった。薬物動態関連遺伝子多型のSNPを解析し、いずれの遺伝子多型もHardy-Weinberg平衡が成立していることを確認した。ABCB1 2677G/TまたはG/Aを保有する患者は、G/Gを保有する患者と比べてアピキサバンのC/D比がわずかに低くなった。ABCG2 421A/A遺伝子を保有する患者は、C/Cを保有する患者と比較してアピキサバンのC/D比が1.55倍有意に高くなった。CYP3A5*1/*3または*3/*3を保有する患者は、*1/*1を保有する患者と比較してアピキサバンのC/D比がそれぞれ1.67倍、1.60倍有意に高くなった。アピキサバンのC/D比は、年齢、Scr、eGFRと有意な相関を示し、eGFRが増加するに伴ってC/D比は低くなった。CYP3A5*3またはABCG2 421A/A保有者、eGFRがアピキサバンのC/D比の変動要因として検出した。
  • 産科危機的出血に伴う搬送のタイミングに苦慮した1例
    川内 華佳, 吉永 洋輔, 大塚 由花, 松浦 寛子, 澁谷 剛志, 堀江 稔, 村上 充剛
    日本周産期・新生児医学会雑誌 53(2) 554-554 2017年06月
  • 表現型・治療方針が異なったSCN5A compound mutationの1家系
    星野健司, 小川潔, 菱谷隆, 河内貞貴, 斎藤千徳, 馬場俊輔, 石川悟, 新田順一, 牧山武, 大野聖子, 堀江稔
    Therapeutic Research 38(4) 362‐365-365 2017年04月
    症例は24歳女性で、中学1年生時の学校心臓検診でQT延長を指摘され、受診した。初診時心電図ではQT=516ms、QTc=520msと著明な延長を認め、運動時のQT短縮は良好であった。SCN5Aのcompound mutation transはE1784K&V1098Lの兄妹例を経験した。異なる表現型を呈したが、表現型に対応する治療により良好な経過を取っている。compound mutationの意義、性差による表現型、重症度の差異を考える上で重要と考えられた。
  • 急性妊娠脂肪肝の周術期にフィブリノゲン濃縮製剤の投与を行った1例
    川内 華佳, 吉永 洋輔, 澁谷 剛志, 松浦 寛子, 大塚 由花, 加藤 雅史, 堀江 稔, 村上 充剛
    東京産科婦人科学会会誌 66(2) 380-386 2017年04月
    急性妊娠脂肪肝(acute fatty liver of pregnancy:AFLP)は主に妊娠後期に発症し重篤な肝機能障害をきたす稀な疾患であり、母児ともに死亡率が高い。重度の凝固障害をきたすことがあり、周術期管理において凝固因子の補充療法が必要となる場合がある。症例は29歳の初産婦で妊娠38週0日の健診時に嘔気と食欲不振を訴えた。肝機能障害、低フィブリノゲン血症、antithrombin-III低下、高度な黄疸を認め、Swansea criteriaからAFLPと臨床診断した。重度の凝固障害を速やかに改善するため、術前にフィブリノゲン濃縮製剤を投与し緊急帝王切開術で児を娩出した。術中の出血量は1032mlであった。AFLPの凝固障害に対するフィブリノゲン濃縮製剤の使用は、新鮮凍結血漿に比して水分の過負荷を避けつつ、短時間に大量のフィブリノゲンを補充でき、術中出血量の減少に寄与する可能性がある。(著者抄録)
  • 心臓突然死の遺伝的背景 ブルガダ症候群におけるSCN5Aコピー数の多様性(Copy Number Variations of SCN5A in Brugada Syndrome)
    園田 桂子, 大野 聖子, 市川 麻理, 服部 哲久, 伊藤 英樹, 牧山 武, 堀江 稔
    日本循環器学会学術集会抄録集 81回 SY09-3 2017年03月
  • 心臓突然死の遺伝的背景 乳児期に診断された先天性QT延長症候群の遺伝的背景とSIDSの乳児における遺伝子変異との比較(Genetic Background of Congenital Long QT Syndrome Diagnosed in Infancy and Comparison of Their Gene Mutations with Those in SIDS)
    堀米 仁志, 吉永 正夫, 住友 直方, 林 立申, 加藤 愛章, 牛ノ濱 大也, 田内 宣生, 大野 聖子, 清水 渉, 堀江 稔, 長嶋 正實
    日本循環器学会学術集会抄録集 81回 SY09-6 2017年03月
  • 症候性QT延長症候群患者で特定されたKCNH2の新規輸送抵抗性変異(A Novel Transport Refractory Mutation in KCNH2 Identified in Symptomatic Long QT Syndrome Patients)
    福本 大介, 大野 聖子, 和田 悠子, 藤居 祐介, 市川 麻理, 福山 恵, 伊藤 英樹, 松浦 博, 堀江 稔
    日本循環器学会学術集会抄録集 81回 PJ-028 2017年03月
  • Inherited primary arrhythmia syndrome患者におけるSCN10Aの稀な一塩基多型(Rare Single Nucleotide Polymorphism of SCN10A in Patients with Inherited Primary Arrhythmia Syndromes)
    福山 恵, 大野 聖子, 市川 麻理, 牧山 武, 堀江 稔
    日本循環器学会学術集会抄録集 81回 PJ-029 2017年03月
  • 経カテーテル的大動脈弁置換術(TAVI)を施行した2例
    山本孝, 八木典章, 松本祐一, 木村紘美, 酒井宏, 堀江稔, 森本政憲, 寺田真也, 坂倉玲欧, 木下武, 鈴木友彰, 浅井徹, 水野隆芳, 北川裕利
    滋賀医学 39 106-106 2017年03月
  • Short‐coupled variant of torsade de pointesの臨床像と遺伝学的背景
    藤居祐介, 伊藤英樹, 大野聖子, 堀江稔, BLANCARD Malorie, GUICHENEY Pascale, 青木寿明, 中川義久, 山本聖, 松井由美恵, 大久保公恵, 渡辺一郎
    滋賀医学 39 73-73 2017年03月
  • 心臓突然死の遺伝的背景(Copy Number Variations of SCN5A in Brugada Syndrome)
    園田 桂子, 大野 聖子, 市川 麻理, 服部 哲久, 伊藤 英樹, 牧山 武, 堀江 稔
    日本循環器学会学術集会抄録集 81回 SY09-3 2017年03月
  • ブルガダ症候群におけるアルコール代謝酵素の遺伝子変異 飲酒後の失神に関する知見(Genetic Variants of Alcohol-Metabolizing Enzymes in Brugada Syndrome: Insights into Syncope after Drinking Alcohol)
    呉 き, 林 秀樹, 牧山 武, 堀江 稔
    日本循環器学会学術集会抄録集 81回 PJ-031 2017年03月
  • 心臓突然死の遺伝的背景(Genetic Background of Congenital Long QT Syndrome Diagnosed in Infancy and Comparison of Their Gene Mutations with Those in SIDS)
    堀米 仁志, 吉永 正夫, 住友 直方, 林 立申, 加藤 愛章, 牛ノ濱 大也, 田内 宣生, 大野 聖子, 清水 渉, 堀江 稔, 長嶋 正實
    日本循環器学会学術集会抄録集 81回 SY09-6 2017年03月
  • 非発作性心房細動に対するExTRaマッピングガイド下非受動興奮領域アブレーション施行後6ヵ月間の経過観察(Six-Month Follow-up after the ExTRa Mappingguided Non-Passive Activation Area Ablation for Non-Paroxysmal Atrial Fibrillation)
    芦原 貴司, 坂田 憲祐, 小澤 友哉, 土谷 健, 原口 亮, 中沢 一雄, 堀江 稔
    日本循環器学会学術集会抄録集 81回 PJ-459 2017年03月
  • A Novel Transport Refractory Mutation in KCNH2 Identified in Symptomatic Long QT Syndrome Patients(和訳中)
    福本 大介, 大野 聖子, 和田 悠子, 藤居 祐介, 市川 麻理, 福山 恵, 伊藤 英樹, 松浦 博, 堀江 稔
    日本循環器学会学術集会抄録集 81回 PJ-028 2017年03月
  • 遺伝性不整脈の日本人コホートにおける遺伝的背景と発症メカニズムの検討
    堀江 稔
    先進医薬研究振興財団研究成果報告集 2016年度 224-228 2017年03月
  • Rare Single Nucleotide Polymorphism of SCN10A in Patients with Inherited Primary Arrhythmia Syndromes(和訳中)
    福山 恵, 大野 聖子, 市川 麻理, 牧山 武, 堀江 稔
    日本循環器学会学術集会抄録集 81回 PJ-029 2017年03月
  • Genetic Variants of Alcohol-Metabolizing Enzymes in Brugada Syndrome: Insights into Syncope after Drinking Alcohol(和訳中)
    呉 き, 林 秀樹, 牧山 武, 堀江 稔
    日本循環器学会学術集会抄録集 81回 PJ-031 2017年03月
  • Six-Month Follow-up after the ExTRa Mappingguided Non-Passive Activation Area Ablation for Non-Paroxysmal Atrial Fibrillation(和訳中)
    芦原 貴司, 坂田 憲祐, 小澤 友哉, 土谷 健, 原口 亮, 中沢 一雄, 堀江 稔
    日本循環器学会学術集会抄録集 81回 PJ-459 2017年03月
  • ラミノパチー患者に対する両室再同期療法は心不全予後を改善させるか?
    中島健三郎, 相庭武司, 西内英, 牧山武, 尾上健児, 鎌倉令, 和田暢, 石橋耕平, 岡村英夫, 大野聖子, 宮本恵宏, 斎藤能彦, 堀江稔, 清水渉, 草野研吾
    日本心臓病学会学術集会(Web) 65th ROMBUNNO.O‐030 (WEB ONLY)-030 2017年09月
  • 当院における超緊急帝王切開12例の検討とシステム構築の現状
    澁谷 剛志, 吉永 洋輔, 大塚 由花, 川内 華佳, 松浦 寛子, 渡辺 昭夫, 加藤 雅史, 堀江 稔, 村上 充剛
    日本産科婦人科学会雑誌 69(2) 772-772 2017年02月
  • マクロproBNP血症の一例
    中川靖章, 錦見俊雄, 錦見俊雄, 酒井宏, 大野聖子, 木下秀之, 稲住英明, 森内健史, 桑原宏一郎, 堀江稔, 木村剛
    日本心血管内分泌代謝学会学術総会プログラム及び抄録集 21st 128 2017年
  • 著明な左室収縮能低下と徐脈を認めplakophilin2遺伝子変異による不整脈原性右室心筋症と診断した1例
    高橋友香里, 久保亨, 越智友梨, 高橋有紗, 宮川和也, 野口達哉, 弘田隆省, 山崎直仁, 堀江稔, 北岡裕章
    日本心臓病学会学術集会(Web) 65th ROMBUNNO.P‐068 (WEB ONLY)-068 2017年09月
  • カテコラミン誘発性多形性心室頻拍の重症化に関与する遺伝な修飾因子の解明
    長谷川奏恵, 長谷川奏恵, 大野聖子, 大野聖子, 伊藤英樹, 芦原貴司, 牧山武, 堀江稔
    心臓 48(12) 1446-1446 2016年12月
  • 無症候の両親にそれぞれSCN5AおよびKCNQ1の変異を認め,異なる遺伝伝達および表現型を示したQT延長症候群の三姉妹例
    古川卓朗, 泉岳, 大野聖子, 堀江稔
    日本小児循環器学会雑誌 33(6) 431‐437(J‐STAGE) 2017年
  • QT延長症候群女性における周産期リスクの検討
    神谷千津子, 石橋耕平, 石橋耕平, 宮崎文, 坂口平馬, 和田暢, 宮本康二, 野田崇, 山内俊史, 伊藤英樹, 大野聖子, 本村秀樹, 小川禎治, 後藤浩子, 南孝臣, 八木原伸江, 渡部裕, 長谷川奏恵, 寺沢彰浩, 三上仁, 荻野佳代, 中野由紀子, 今城沙都, 福嶋遥佑, 都築慶光, 朝倉こう子, 吉松淳, 白石公, 宮本恵宏, 安田聡, 堀江稔, 清水渉, 清水渉, 草野研吾, 相庭武司
    日本人類遺伝学会大会プログラム・抄録集 62nd 333 2017年
  • 重症新生児仮死児の高次医療機関への迅速な搬送を目指した取り組み
    藤田 基資, 野村 智章, 西村 直人, 釜江 智佳子, 金井 貴志, 中川 紀子, 滝沢 真理, 川内 華佳, 渋谷 剛志, 加藤 雅史, 吉永 洋輔, 堀江 稔, 村上 充剛, 黒木 康富
    防衛衛生 64(別冊) 48-48 2016年12月
  • 脳性ナトリウム利尿ペプチド(BNP),N末端プロBNP(NT‐proBNP)の最新情報
    蔦本尚慶, 市川麻理, 河原千穂, 酒井宏, 堀江稔
    日本心不全学会学術集会プログラム・抄録集 21st 249 2017年
  • 今,診断を見直す 血中BNP値やNT‐proBNP値を用いた心不全診療の留意点
    蔦本尚慶, 奥山雄介, 福山恵, 河原千穂, 酒井宏, 堀江稔
    循環plus 17(1) 10‐12-12 2016年10月
  • 滋賀医科大学附属病院におけるアミオダロンによる間質性肺炎
    林秀樹, 伊藤英樹, 芦原貴司, 小澤友哉, 加藤浩一, 藤居祐介, 坂田憲祐, 堀江稔
    Progress in Medicine 36(Suppl.1) 439‐442-442 2016年04月
    アミオダロンによる間質性肺炎について検討した。アミオダロン使用例のうち間質性肺炎と診断された患者を抽出した。アミオダロンを使用した448例中、5例(男性3名、女性2名、平均72±5歳)で間質性肺炎を認めた。KL-6は多くの症例が正常範囲内であったが、間質性肺炎5例中2例は正常値以上であった。間質性肺炎3例で白血球数、また4例でCRP値が正常値以上であった。AST値、ALT値ともに正常値以上のアミオダロン使用例はいたが、間質性肺炎5例では正常範囲内であった。また、総ビリルビン値、直接ビリルビン値が正常値以上のアミオダロン使用例もいた。膵炎マーカーのアミラーゼが正常値以上のアミオダロン使用例もいた。TSH値、fT3値、fT4値が正常値以上のアミオダロン使用例がいた。
  • 日本循環器学会/日本小児循環器学会合同ガイドライン 2016年版 学校心臓検診のガイドライン
    住友 直方, 石川 広己, 泉田 直己, 市田 蕗子, 岩本 眞理, 笠巻 祐二, 久賀 圭祐, 土井 庄三郎, 中西 敏雄, 馬場 礼三, 檜垣 高史, 堀米 仁志, 三谷 義英, 武者 春樹, 吉永 正夫, 阿部 勝己, 鮎沢 衛, 牛ノ濱 大也, 太田 邦雄, 加藤 愛章, 加藤 太一, 澤田 博文, 鉾碕 竜範, 葭葉 茂樹, 新 博次, 小川 俊一, 奥村 謙, 筒井 裕之, 長嶋 正實, 丹羽 公一郎, 平山 篤志, 堀江 稔, 日本循環器学会,日本小児循環器学会,一般社団法人日本循環器学会ガイドライン委員会
    循環器病ガイドシリーズ 2016(学校心臓検診のガイドライン) i-80 2016年11月
  • 日本循環器学会/日本小児循環器学会合同ガイドライン【ダイジェスト版】 2016年版 学校心臓検診のガイドライン
    住友 直方, 石川 広己, 泉田 直己, 市川 蕗子, 岩本 眞理, 笠巻 祐二, 久賀 圭祐, 土井 庄三郎, 中西 敏雄, 馬場 礼三, 檜垣 高史, 堀米 仁志, 三谷 義英, 武者 春樹, 吉永 正夫, 阿部 勝己, 鮎沢 衛, 牛ノ濱 大也, 太田 邦雄, 加藤 愛章, 加藤 太一, 澤田 博文, 鉾碕 竜範, 葭葉 茂樹, 新 博次, 小川 俊一, 奥村 謙, 筒井 裕之, 長嶋 正實, 丹羽 公一郎, 平山 篤志, 堀江 稔, 日本循環器学会,日本小児循環器学会
    循環器病ガイドシリーズ 2016(学校心臓検診のガイドライン) 81-148 2016年11月
  • ホルター心電図で2方向性心室頻拍を認めたアンダーセン・タウィル症候群の1例
    大国 千尋, 清水 祥子, 木村 紘美, 藤澤 義久, 堀江 稔, 宮平 良満, 九嶋 亮治
    医学検査 65(6) 684-684 2016年11月
    アンダーセン・タウィル症候群(Andersen-Tawil syndrome;ATS)は、(1)U波を伴う心室性不整脈、(2)周期性四肢麻痺、(3)外表小奇形を3徴とするまれな遺伝性疾患である。内向き整流性カリウムチャネルであるKir2.1蛋白をコードしているKCNJ2遺伝子の変異が原因で発症する。心電図所見としてQU延長を伴う著明なU波と頻発する心室期外収縮(PVC)、2方向性心室頻拍を認め、治療にはIc群抗不整脈薬であるフレカイニドの有用性が報告されている。症例は50代女性、ATSの3徴全てを満たし、QU延長(723msec)を伴う著明なU波、PVC頻発を認め、遺伝子検索にてKCNJ2遺伝子変異陽性であった。ホルター心電図では総心拍の24%のPVC、2方向性心室頻拍を認め、フレカイニドの導入により9%までPVCが減少、動悸症状も改善した。ATSでは、増高したU波や2方向性心室頻拍が重要な所見となるため、心電図検査、ホルター心電図の解析では、QU時間、U波高、U波幅、PVCの極性などの情報にも着目する必要がある。(著者抄録)
  • Desmosome2遺伝子に非常に稀少な1塩基置換2座を認めた不整脈原性右室心筋症(ARVC)の1例
    利根川 玲奈, 中島 崇智, 高橋 弘武, 村上 彰通, 仲野 陽介, 大野 聖子, 和田 悠子, 宮本 敬史, 堀江 稔, 武藤 誠
    日本内科学会関東地方会 628回 35-35 2016年11月
  • 心房細動合併収縮不全の1例~Rate control?rhythm control?それとも...~
    酒井宏, 冨田行則, 小澤友哉, 山本孝, 堀江稔
    滋賀医学 38 109-109 2016年03月
  • AMIによる難治性VFに対し病病連携とROSC後の集学的治療により社会復帰した一例
    田中智基, 村尾淳司, 喜多理香, 北村直美, 松下美季子, 八木典章, 山本孝, 堀江稔, 藤野和典, 田畑貴久, 江口豊, 岡林旅人
    滋賀医学 38 104‐105-105 2016年03月
  • 小児QT延長症候群:LQT2は発症年齢が高いが重症例が多い
    小澤淳一, 大野聖子, 伊藤英樹, 堀江稔, 大野聖子, 小澤淳一, 牧山武
    滋賀医学 38 71-71 2016年03月
  • ペースメーカ,ICD,CRTを受けた患者の社会復帰・就学・就労に関するガイドライン(2013年改訂版)
    奥村謙, 青沼和隆, 安部治彦, 鎌倉史郎, 清水昭彦, 住友直方, 新田隆, 野島俊雄, 萩原誠久, 堀江正知, 江島浩一郎, 大森裕也, 荻ノ沢泰司, 神山浩, 佐々木真吾, 副島京子, 中島博, 野田崇, 吉賀康裕, 渡辺重行, 加藤貴雄, 田邉晃久, 土肥誠太郎, 平山篤志, 堀江稔
    日本心臓血管外科学会雑誌 45(2) (1)‐(23) 2016年03月
  • 日本循環器学会/日本TDM学会合同ガイドライン(2013-2014年度合同研究班報告)【ダイジェスト版】 2015年版 循環器薬の薬物血中濃度モニタリングに関するガイドライン
    青沼 和隆, 志賀 剛, 新 博次, 池田 隆徳, 市田 蕗子, 上野 和行, 越前 宏俊, 栄田 敏之, 清水 渉, 菅原 満, 土下 喜正, 土岐 浩介, 戸塚 恭一, 萩原 誠久, 長谷川 純一, 林 秀晴, 平尾 見三, 前田 頼伸, 松本 直樹, 渡邉 英一, 笠井 英史, 篠原 徳子, 杉山 篤, 鈴木 敦, 住友 直方, 関口 幸夫, 高橋 尚彦, 野上 昭彦, 橋口 正行, 平田 純生, 松本 宜明, 湯川 栄二, 伊藤 宏, 井上 博, 大江 透, 篠崎 公一, 田中 一彦, 本間 真人, 堀江 稔, 三浦 崇則, 日本循環器学会,日本TDM学会
    TDM研究 33(3) 123-157 2016年09月
  • 当院における心臓手術後リハビリテーション進行の検討 成長期に入った当院における今後の課題
    飛田 良, 澁川 武志, 木下 妙子, 前川 昭次, 川口 民郎, 浅井 徹, 堀江 稔
    心臓リハビリテーション 22(1) 44-50 2016年06月
    【目的】導入期から成長期に入った当院における心臓手術後リハビリテーションの進行状況を把握し、今後の課題を検討すること。【方法】平成24年4月から平成25年8月までの当院心臓血管外科手術症例469例を緊急群と待機群で各々歩行獲得状況が早期自立群、順調群、遅延群、非自立群の4群に分け、日本循環器学会ガイドラインが示すものと比較検討した。【結果】待機群に比べ緊急群の術後歩行自立日数は有意に延長していた。術後歩行獲得状況は、待機群でガイドラインよりも早期自立群が多く、緊急群では、ガイドラインよりも非自立群が多く、大血管手術が多数を占め、肺炎や長期挿管などの呼吸器由来が主な遅延理由であった。【結論】当院における今後の課題は、ハイリスク症例への効果的介入であり、早期離床や一般的な運動療法だけでなく、CCUや一般病棟での多職種での関わりをより深め、術後早期からの効果的介入が重要になると考える。(著者抄録)
  • 日本循環器学会/日本TDM学会合同ガイドライン(2013-2014年度合同研究班報告)【ダイジェスト版】 2015年版 循環器薬の薬物血中濃度モニタリングに関するガイドライン
    青沼 和隆, 志賀 剛, 新 博次, 池田 隆徳, 市田 蕗子, 上野 和行, 越前 宏俊, 栄田 敏之, 清水 渉, 菅原 満, 土下 喜正, 土岐 浩介, 戸塚 恭一, 萩原 誠久, 長谷川 純一, 林 秀晴, 平尾 見三, 前田 頼伸, 松本 直樹, 渡邉 英一, 笠井 英史, 篠原 徳子, 杉山 篤, 鈴木 敦, 住友 直方, 関口 幸夫, 高橋 尚彦, 野上 昭彦, 橋口 正行, 平田 純生, 松本 宜明, 湯川 栄二, 伊藤 宏, 井上 博, 大江 透, 篠崎 公一, 田中 一彦, 本間 真人, 堀江 稔, 三浦 崇則, 日本循環器学会,日本TDM学会
    TDM研究 33(3) 123-157 2016年09月
  • 慢性心房細動アブレーションにおけるイノベーション実現に向けたin silicoの挑戦―ExTRa Mappingの開発―
    芦原貴司, 坂田憲祐, 小澤友哉, 土谷健, 原口亮, 稲田慎, 中沢一雄, 堀江稔
    心電図 36(Supplement 1) 52-1 2016年02月
  • 先天性QT延長症候群におけるmicrovolt T wave alternans
    林秀樹, 大野聖子, 清水祥子, 藤澤義久, 泉裕美, 石垣多佳子, 西川達也, 大国千尋, 堀江稔
    心電図 36(Supplement 1) 23-1 2016年02月
  • 遺伝性心筋疾患の現状と展望を識る 6 不整脈原性右室心筋症
    和田悠子, 堀江稔
    Heart View 20(2) 142‐150 2016年02月
  • 慢性心房細動に治療標的となるような定在ローターは存在するか?―ExTRa Mappingによる臨床的観察研究―
    坂田憲祐, 芦原貴司, 小澤友哉, 土谷健, 原口亮, 稲田慎, 中沢一雄, 堀江稔
    心電図 36(Supplement 1) 62-1 2016年02月
  • 突然死を識る・治す【イオンチャネル病における突然死】QT短縮症候群
    堀江稔
    医学のあゆみ 256(6) 647‐651 2016年02月
  • 循環器疾患と突然死 遺伝性不整脈と突然死
    堀江稔
    循環器内科 79(2) 95‐101-101 2016年02月
  • 【不整脈を科学する】 突然死を識る・治す イオンチャネル病における突然死 QT短縮症候群
    堀江 稔
    医学のあゆみ 256(6) 647-651 2016年02月
    QT短縮症候群(SQTS)は、12誘導心電図上の著しく短いQT時間と心室細動(VF)による突然死を特徴とする遺伝性不整脈である。心電図上、はじめて記載されたのは21世紀になってからであり、比較的最近発見された病気である。基礎心疾患を認めず、突然死の家族歴があり、心房細動(AF)を高率に合併する。また、乳幼児突然死症候群(SIDS)の一因と考えられている。イオンチャネル病の一種で、これまでKチャネルやCaチャネルの異常が報告されている。治療の第一選択は植込み型除細動器(ICD)であり、補助療法としてキニジン内服が有効である。発症頻度の低い疾患であり、その病像もまだ不明な点が多く、今後のさらなる症例の蓄積による病態の解明が期待される。(著者抄録)
  • 【遺伝性心筋疾患の現状と展望を識る】 識る 不整脈原性右室心筋症
    和田 悠子, 堀江 稔
    Heart View 20(2) 142-150 2016年02月
  • 日本循環器学会/日本TDM学会合同ガイドライン(2013-2014年度合同研究班報告) 2015年版 循環器薬の薬物血中濃度モニタリングに関するガイドライン
    青沼 和隆, 志賀 剛, 新 博次, 池田 隆徳, 市田 蕗子, 上野 和行, 越前 宏俊, 栄田 敏之, 清水 渉, 菅原 満, 土下 喜正, 土岐 浩介, 戸塚 恭一, 萩原 誠久, 長谷川 純一, 林 秀晴, 平尾 見三, 前田 頼伸, 松本 直樹, 渡邉 英一, 笠井 英史, 篠原 徳子, 杉山 篤, 鈴木 敦, 住友 直方, 関口 幸夫, 高橋 尚彦, 野上 昭彦, 橋口 正行, 平田 純生, 松本 宜明, 湯川 栄二, 伊藤 宏, 井上 博, 大江 透, 篠崎 公一, 田中 一彦, 本間 真人, 堀江 稔, 三浦 崇則, 日本循環器学会,日本TDM学会
    循環器病ガイドシリーズ 2015(循環器薬の薬物血中濃度モニタリングに関するガイドライン) 3-54 2016年02月
  • 日本循環器学会/日本TDM学会合同ガイドライン(2013-2014年度合同研究班報告)【ダイジェスト版】2015年版 循環器薬の薬物血中濃度モニタリングに関するガイドライン
    青沼 和隆, 志賀 剛, 新 博次, 池田 隆徳, 市田 蕗子, 上野 和行, 越前 宏俊, 栄田 敏之, 清水 渉, 菅原 満, 土下 喜正, 土岐 浩介, 戸塚 恭一, 萩原 誠久, 長谷川 純一, 林 秀晴, 平尾 見三, 前田 頼伸, 松本 直樹, 渡邉 英一, 笠井 英史, 篠原 徳子, 杉山 篤, 鈴木 敦, 住友 直方, 関口 幸夫, 高橋 尚彦, 野上 昭彦, 橋口 正行, 平田 純生, 松本 宜明, 湯川 栄二, 伊藤 宏, 井上 博, 大江 透, 篠崎 公一, 田中 一彦, 本間 真人, 堀江 稔, 三浦 崇則, 日本循環器学会,日本TDM学会
    循環器病ガイドシリーズ 2015(循環器薬の薬物血中濃度モニタリングに関するガイドライン) 55-89 2016年02月
  • 心エコー検査で肥大型心筋症に伴う巨大心尖部瘤を認めた1例
    上田啓介, 八木典章, 山本孝, 林秀樹, 堀江稔
    日本循環器学会近畿地方会(Web) 121st KINKI121,P01 (WEB ONLY) 2016年
  • 運動中に心肺停止になった不整脈源性右室心筋症(ARVC)の一例
    鳥居さゆ希, 坂田憲祐, 川口民郎, 酒井宏, 小澤友哉, 大野聖子, 芦原貴司, 伊藤英樹, 堀江稔
    日本循環器学会近畿地方会(Web) 121st KINKI121,A22 (WEB ONLY) 2016年
  • A型急性大動脈解離の吻合部仮性瘤による慢性的DICに伴うCRT‐Dポケット血腫の治療に難渋した症例
    岡本寛樹, 小澤友哉, 山本孝, 芦原貴司, 堀江稔, 浅井徹, 鈴木友彰, 坂倉玲欧
    日本循環器学会近畿地方会(Web) 122nd KINKI122,A06 (WEB ONLY) 2016年
  • 精巣腫瘍に対するBEP療法中に認めた急性心筋梗塞の1例
    中島健太, 八木典章, 松本祐一, 山本孝, 堀江稔
    日本循環器学会近畿地方会(Web) 122nd KINKI122,C37 (WEB ONLY) 2016年
  • 小児期心筋症の心電図学的抽出基準,心臓超音波学的診断基準の作成と遺伝学的検査を反映した診療ガイドラインの作成に関する研究 心筋症患児情報の収集と抽出基準・診断基準の作成に関する研究―1次調査結果について―
    吉永正夫, 堀米仁志, 大野聖子, 市田蕗子, 住友直方, 長嶋正實, 緒方裕光, 堀江稔, 蒔田直昌, 牛ノ濱大也, 田内宣生, 佐藤誠一, 高橋秀人, 岩本眞理, 太田邦雄, 立野滋, 泉田直己, 畑忠善, 小垣滋豊, 安田和志, 西原栄起, 野村裕一, 江口太助, 鮎沢衛
    小児期心筋症の心電図学的抽出基準、心臓超音波学的診断基準の作成と遺伝学的検査を反映した診療ガイドラインの作成に関する研究 平成27年度 総括・分担研究報告書 51‐60 2016年
  • 遺伝子診断に基づく不整脈疾患群の病態解明および診断基準・重症度分類・ガイドライン作成に関する研究
    堀江稔
    遺伝子診断に基づく不整脈疾患群の病態解明および診断基準・重症度分類・ガイドライン作成に関する研究 平成27年度 総括研究報告書 1‐5 2016年
  • 小児期心筋症の心電図学的抽出基準,心臓超音波学的診断基準の作成と遺伝学的検査を反映した診療ガイドラインの作成に関する研究 健常小児の心臓超音波所見の基準値作成に関する研究
    吉永正夫, 堀米仁志, 大野聖子, 市田蕗子, 住友直方, 長嶋正實, 緒方裕光, 堀江稔, 蒔田直昌, 牛ノ濱大也, 田内宣生, 佐藤誠一, 高橋秀人, 岩本眞理, 太田邦雄, 立野滋, 泉田直己, 畑忠善, 小垣滋豊, 安田和志, 西原栄起, 野村裕一, 江口太助, 鮎沢衛
    小児期心筋症の心電図学的抽出基準、心臓超音波学的診断基準の作成と遺伝学的検査を反映した診療ガイドラインの作成に関する研究 平成27年度 総括・分担研究報告書 34‐50 2016年
  • CALM遺伝子変異によるQT延長症候群の患者由来iPS細胞を用いた疾患モデルにおける変異アレル特異的ノックアウトによる治療的アプローチ
    山本雄大, 牧山武, 張田健志, 佐々木健一, 早野護, 西内英, ウリヤンハイ イミン, 糀谷泰彦, 廣瀬紗也子, チン カヨウ, 石川泰輔, 大野聖子, 蝶名林和久, 吉田善紀, 堀江稔, 蒔田直昌, 木村剛
    日本分子生物学会年会プログラム・要旨集(Web) 39th ROMBUNNO.1P‐0016 (WEB ONLY) 2016年
  • 心不全患者のエネルギー代謝に関する臨床研究
    山内 宏美, 佐々木 雅也, 高岡 あずさ, 大井 彰子, 栗原 美香, 中西 直子, 山本 孝, 堀江 稔, 鈴木 友彰, 浅井 徹, 小松 龍史
    日本病態栄養学会誌 19(Suppl.) S-125 2015年12月
  • 慢性心房細動のアブレーション治療におけるイノベーション創出に向けたin silicoの挑戦
    芦原貴司, 小澤友哉, 坂田憲祐, 土谷健, 原口亮, 稲田慎, 中沢一雄, 堀江稔
    日本コンピュータ外科学会誌 17(3) 155 2015年10月
  • ファーマコゲノミクス検査システムの構築と評価
    赤羽理也, 野田哲史, 磯野哲一郎, 池田義人, 平大樹, 森田真也, 堀江稔, 寺田智祐
    日本医療薬学会年会講演要旨集 25th 205 2015年10月
  • 遺伝性不整脈の治療戦略 Brugada症候群と早期再分極症候群(J波症候群)の薬物療法
    林秀樹, 堀江稔
    心電図 35(2) 95-103 2015年10月
    Brugada症候群と早期再分極症候群は、心室細動(VF)を発症し突然死を起こす可能性がある。両症候群は、心電図でST上昇(J波)を認める。その主な機序として、一過性外向き電流(Ito)の増加が考えられている。キニジンに代表されるItoを抑制する薬剤はVFの発生を抑制するとの報告があり、同時にJ波を消失させることも明らかにされている。このような薬剤は、Brugada症候群と早期再分極症候群において植込み型除細動器施行後のVFに対する補助的治療として使用される。本論文では、Brugada症候群と早期再分極症候群に対して有効な薬剤の作用機序を解説し、薬物療法の既報についてまとめる。(著者抄録)
  • コンピュータ外科の新展開 次世代のキーテクノロジー 慢性心房細動のアブレーション治療におけるイノベーション創出に向けたin silicoの挑戦
    芦原 貴司, 小澤 友哉, 坂田 憲祐, 土谷 健, 原口 亮, 稲田 慎, 中沢 一雄, 堀江 稔
    日本コンピュータ外科学会誌 17(3) 155-155 2015年10月
  • 蘇生時の心電図から診断したカテコラミン誘発性多形性心室頻拍の4歳児例
    木村 翔, 本田 隆文, 平井 希, 保科 しほ, 浜田 洋通, 川村 美朋子, 堀江 稔, 寺井 勝
    日本集中治療医学会雑誌 22(5) 439-442 2015年09月
    症例は4歳、男児。既往歴や家族歴は特にない。外出しようとした玄関先で失神し、9分後救急隊車内収容時に心肺停止であったため蘇生が開始された。心停止から30分で自己心拍が再開した。蘇生時の頻回の多形性心室頻拍と、それに続く心室細動からカテコラミン誘発性多形性心室頻拍(catecholaminergic polymorphic ventricular tachycardia、CPVT)を疑い、遺伝子検査で常染色体劣性遺伝のcalsequestrin 2(CASQ2)遺伝子異常を2ヶ所認め、確定診断に至った。神経学的後遺症を残したものの、現在β遮断薬内服で再発作を認めず管理している。診断や薬効評価に関して、幼児では運動負荷検査の実施が難しいため、ホルター心電計装着下で家族と共に運動させるなどの工夫が必要である。(著者抄録)
  • 遺伝子変異が同定された徐脈性不整脈の3例
    福岡哲哉, 漆畑伶, 原周平, 小松賢司, 塩田勉, 水谷真一郎, 佐藤恵, 森下雄大, 杉浦崇浩, 大久保由美子, 長谷部秀幸, 鶴井聡, 大野聖子, 堀江稔
    日本小児科学会雑誌 119(9) 1425-1425 2015年09月
  • 遺伝性心疾患の遺伝子診断を日常診療にどう生かすか QT延長症候群の遺伝子診断と臨床への活用
    大野 聖子, 堀江 稔
    日本心臓病学会学術集会抄録 63回 678-678 2015年09月
  • 運動時における失神症例からのカテコラミン誘発性多形性心室頻拍症例の抽出
    小澤淳一, 小澤淳一, 大野聖子, 大野聖子, 藤居祐介, 牧山武, 鈴木博, 齋藤昭彦, 堀江稔
    日本小児循環器学会雑誌 31(Supplement 1) S1.209-209 2015年07月
  • 完全房室ブロックに伴いTorsade de Pointesを来たし、Tpeak-Tend延長が発作予測に有効であることが示唆された一例
    諸戸 礼知安, 加藤 浩一, 藤居 祐介, 小澤 友哉, 芦原 貴司, 伊藤 英樹, 堀江 稔
    日本心臓病学会学術集会抄録 63回 1132-1132 2015年09月
  • バイオマーカーとRAS 心不全とRASバイオマーカー
    蔦本尚慶, 酒井宏, 服部哲久, 河原千穂, 堀江稔
    Angiotensin Research 12(4) 220‐224-224 2015年10月
    心不全とRASバイオマーカーの歴史は、心不全大規模臨床試験の結果からはじまったといっても過言ではない。レニン・アンジオテンシン・アルドステロン系(RAAS)や交感神経系の経路を遮断することによって、心保護作用を増強させる薬剤が慢性心不全の予後を改善することが証明されるに至り、慢性心不全の発症進展には、神経体液性因子のバランスの破綻が重要な因子であることが証明され、現在では収縮不全患者の標準治療薬として、ACE阻害薬/ARB、β遮断薬、アルドステロン拮抗薬が使用されている。2014年にPARADIGM-HFが発表されて、再びこの領域が注目を集めており解説する。(著者抄録)
  • PKP2遺伝子変異が同定された不整脈源性右室心筋症の1剖検例
    松本祐一, 長岡伊織, 伊藤英樹, 伊藤誠, 杉原洋行, 川嶋剛史, 堀江稔
    心電図 35(1) 31-38 2015年07月
    症例は29歳、男性。2001年、24歳時に健診で心室期外収縮の頻発と非持続性心室頻拍を指摘され当科で精査したところ、不整脈源性右室心筋症(arrhythmogenic right ventricular cardiomyopathy:ARVC)と診断され、β遮断薬の投与と運動制限により、その後は症状なく安定して経過していた。しかし2006年3月、29歳時に激しい運動の直後に心室細動となり、ただちにby-stander CPRを開始されて近医へ搬送されたが、死亡した。剖検によりARVCに合致する所見が認められ、また心室細動の原因として考えうるその他の所見は認められなかった。当科で行ったARVC関連遺伝子の検索により、plakophilin-2(PKP2)をコードする遺伝子PKP2の変異(c.C2119T、p.Q707X)が認められた。PKP2はデスモゾームの構成蛋白であり、この遺伝子異常により細胞間接着に異常を生じたため、ARVCをきたしたと考えられた。PKP2遺伝子変異が同定されたARVCの剖検症例は貴重と考えられたので報告する。(著者抄録)
  • 左室機能障害を伴う高速AFとVTに対する超短期作用型β1選択的遮断薬であるlandiololの臨床利用可能性(Practical Applicability of Landiolol, an Ultra-short-acting β 1-selective Blocker, for Rapid AF and VT with Left Ventricular Dysfunction)
    和田 悠子, 相庭 武司, 辻田 靖之, 伊藤 英樹, 和田 暢, 中島 育太郎, 石橋 耕平, 宮本 康二, 野田 崇, 菅野 康夫, 神崎 秀明, 安斉 俊久, 草野 研吾, 安田 聡, 堀江 稔, 小川 久雄
    日本心臓病学会学術集会抄録 63回 1357-1357 2015年09月
  • In SilicoヒトiPS細胞由来心筋細胞の構築と不整脈研究への応用可能性
    芦原貴司, 黒川洵子, 諫田泰成, 関野祐子, 原口亮, 稲田慎, 中沢一雄, 堀江稔
    日本小児循環器学会雑誌 31(Supplement 1) S1.103 2015年07月
  • 新しいシミュレーション医学の小児循環器医療への応用 In SilicoヒトiPS細胞由来心筋細胞の構築と不整脈研究への応用可能性
    芦原 貴司, 黒川 洵子, 諫田 泰成, 関野 祐子, 原口 亮, 稲田 慎, 中沢 一雄, 堀江 稔
    日本小児循環器学会雑誌 31(Suppl.1) s1-103 2015年07月
  • カテコラミン感受性多形性心室頻拍CPVTに対する当院での治療経験
    倉岡 彩子, 牛ノ濱 大也, 井福 俊充, 中村 真, 佐川 浩一, 石川 司朗, 住友 直方, 大野 聖子, 堀江 稔
    日本小児循環器学会雑誌 31(Suppl.1) s1-209 2015年07月
  • 循環器疾患の発症とモザイク
    長谷川奏恵, 大野聖子, 堀江稔
    循環器内科 77(4) 391-395 2015年04月
  • 多階層生体機能学の創成に向けたシミュレーション研究の成果と進展=ヒトiPS細胞由来心筋細胞シートの不整脈研究への応用可能性:in silico不整脈学の観点から
    芦原貴司, 黒川洵子, 諫田泰成, 原口亮, 稲田慎, 中沢一雄, 堀江稔
    生体医工学 53(3) 100-105 2015年06月
  • Clinical efficacy of thrombus aspiration on 5-year clinical outcomes in patients with ST-segment elevation acute myocardial infarction undergoing percutaneous coronary intervention
    Hiroki Watanabe, Hiroki Shiomi, Kenji Nakatsuma, Takeshi Morimoto, Tomohiko Taniguchi, Yutaka Furukawa, Yoshihisa Nakagawa, Minoru Horie, Takeshi Kimura, Takeshi Kimura, Ryuzo Sakata, Akira Marui, Mitsuo Matsuda, Hirokazu Mitsuoka, Masahiko Onoe, Yoshihisa Nakagawa, Kazuo Yamanaka, Hisayoshi Fujiwara, Yoshiki Takatsu, Nobuhisa Ohno, Ryuji Nohara, Tomoyuki Murakami, Teruki Takeda, Masakiyo Nobuyoshi, Masashi Iwabuchi, Michiya Hanyu, Ryozo Tatami, Tsutomu Matsushita, Manabu Shirotani, Noboru Nishiwaki, Toru Kita, Yutaka Furukawa, Yukikatsu Okada, Hiroshi Kato, Hiroshi Eizawa, Katsuhisa Is, Masaru Tanaka, Shogo Nakayama, Jong Dae Lee, Akira Nakano, Takaaki Koshiji, Koichi Morioka, Akinori Takizawa, Mitsuomi Shimamoto, Fumio Yamazaki, Masaaki Takahashi, Junichiro Nishizawa, Minoru Horie, Hiroyuki Takashima, Takashi Tamura, Masaki Aota, Mamoru Takahashi, Takafumi Tabata, Chuwa Tei, Shuichi Hamasaki, Yutaka Imoto, Hiroyuki Yamamoto, Hirofumi Kambara, Osamu Doi, Katsuhiko Matsuda, Masafumi Nara, Kazuaki Mitsudo, Kazushige Kadota, Tatsuhiko Komiya, Shinji Miki, Tetsu Mizoguchi, Hiroyuki Nakajima, Hisao Ogawa, Seigo Sugiyama, Michio Kawasuji, Syuji Moriyama, Ryuichi Hattori, Takeshi Aoyama, Makoto Araki, Satoru Suwa, Keiichi Tanbara, Kumiko Kitagawa, Misato Yamauchi, Naoko Okamoto, Yumika Fujino, Saori Tezuka, Asuka Saeki, Miya Hanazawa, Yuki Sato, Chikako Hibi, Hitomi Sasae, Emi Takinami, Yuriko Uchida, Yuko Yamamoto, Satoko Nishida, Mai Yoshimoto, Sachiko Maeda, Izumi Miki, Saeko Minematsu, Mitsuru Abe, Hiroki Shiomi, Tomohisa Tada, Junichi Tazaki, Yoshihiro Kato, Mamoru Hayano
    Journal of the American Heart Association 4 2015年06月
    © 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. BACKGROUND: Adjunctive thrombus aspiration (TA) during primary percutaneous coronary intervention (PCI) was reported to promote better coronary and myocardial reperfusion. However, long-term mortality benefit of TA remains controversial. The objective of this study is to investigate the clinical impact of TA on long-term clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI. METHODS AND RESULTS: The CREDO-Kyoto AMI Registry is a large-scale cohort study of acute myocardial infarction patients undergoing coronary revascularization in 2005-2007 at 26 hospitals in Japan. Among 5429 patients enrolled in the registry, the current study population consisted of 3536 patients who arrived at the hospital within 12 hours after the symptom onset and underwent primary PCI. Clinical outcomes were compared between the 2 patient groups with or without TA. During primary PCI procedures, 2239 out of 3536 (63%) patients underwent TA (TA group). The cumulative 5-year incidence of all-cause death was significantly lower in the TA group than in the non-TA group (18.5% versus 23.9%, log-rank P < 0.001). After adjusting for confounders, however, the risk for all-cause death in the TA group was not significantly lower than that in the non-TA group (hazard ratio: 0.90, 95% CI: 0.76 to 1.06, P=0.21). The adjusted risks for cardiac death, myocardial infarction, stroke, and target-lesion revascularization were also not significantly different between the 2 groups. CONCLUSIONS: Adjunctive TA during primary PCI was not associated with better 5-year mortality in STEMI patients.
  • Genetic basis of early repolarization syndrome
    Minoru Horie, Keiko Sonoda, Seiko Ohno
    J Wave Syndromes: Brugada and Early Repolarization Syndromes 77-90 2016年01月
    © Springer International Publishing Switzerland 2016. Among patients with idiopathic ventricular fibrillation (IVF), we experienced significantly higher prevalence of early repolarization (ER), which had been considered as a benign ECG finding in the past. In addition, recurrence of fatal ventricular arrhythmia was associated with the presence of ER. In analogy to ER seen in Brugada syndrome (BS), recently, a novel concept for J-wave syndrome (JWS) has been proposed by Dr. Antzelevitch and Dr. Yan, which includes both BS and ER syndrome (ERS). Indeed, there are several clinical similarities between them regarding (1) presence of familial cases, (2) male predominance, (3) predominant VF occurrence in night, (4) bradycardia-induced augmentation of J-point elevation, (5) reduction or elimination of J-point elevation during exercise or atrial fibrillation, and (6) pharmacological usefulness of isoproterenol and quinidine. From the point of genetic basis, there reported several candidate genes responsible for ERS, most of which are overlapped with those associated with Brugada syndrome. This chapter will mainly focus on the genetic background of ERS and discuss its similarity and difference to that in BS.
  • 循環器疾患と分子遺伝学 総説:先制医療としての遺伝子診断と循環器病
    堀江稔
    循環器内科 77(4) 289-293 2015年04月
  • Novel SCN10A variants associated with Brugada syndrome
    Megumi Fukuyama, Seiko Ohno, Seiko Ohno, Seiko Ohno, Takeru Makiyama, Minoru Horie
    Europace 18(6) 905-911 2016年01月
    © The Author 2015. Aims The expression of sodium channel Nav1.8 in cardiac nervous systems has been identified, and variants of SCN10A that encodes Nav1.8 contribute to the development of Brugada syndrome (BrS) by modifying the function of Nav1.5 or directly reducing the sodium current. The aim of this study was to identify the frequency of SCN10A mutations in Japanese patients with BrS and to compare the phenotypical differences between patients with BrS and those who have other BrScausative genes. Methods and results This study involved 240 Japanese probands who were clinically suspected with BrS and were negative for mutations in major BrS-related genes.We screened for the SCN10A gene using a high-resolution melting method and direct sequencing. In addition, we compared the clinical characteristics among the probands with gene mutations in SCN10A, 6 probands with CACNA1C and 17 probands with SCN5A.We identified six SCN10A variant carriers (2.5%): W189R, R844H (in two unrelated probands), N1328K, R1380Q, and R1863Q. Fivewere male. Fourwere symptomatic: one died following sudden cardiopulmonary arrest at age 35, one suffered ventricular fibrillation, and two had recurrent syncope. Compared with BrS patients carrying SCN5A or CACNA1C mutations, although there were no significant differences among them, symptomatic patients in the SCN10A group tended to be older than those in the other gene groups. Conclusion In six BrS probands who carried SCN10Avariants, most experienced severe arrhythmic attacks. It is of clinical importance to screen SCN10A mutations in BrS, although the functional significance of these variants remains unclear.
  • 左室心外膜側に頻拍の起源を同定し56穴Irrigation Catheterによる心内膜側からの通電にて心内外膜共通回路の完全離断に成功した陳旧性心筋梗塞の1例
    小澤 友哉, 芦原 貴司, 藤居 祐介, 伊藤 英樹, 杉本 喜久, 伊藤 誠, 堀江 稔, 青沼 和隆
    臨床心臓電気生理 38 229-237 2015年05月
    前壁陳旧性心筋梗塞後(OMI)の経過中に持続性心室頻拍(VT)を発症し2010年ICD植込み術を施行。以降、OMI-VTに対し二度のアブレーションの施行でもVTの再発を認めICDが作動。2013年に3rd sessionが必要となった症例である。3rd sessionでは前室間溝静脈(AIV)内に多極カテーテルを挿入し心外膜側で洞調律下に遅延電位(ILP)を確認した。同部のペーシング時の波形はstim-QRS時間は著しく延長しclinical VT波形と一致した。右室の頻回刺激にてclinical VTが誘発された。VTは心外膜側と心内膜側に共通回路をもち旋回していた。VT中に心外膜側の遅延電位確認部位での局所電位では拡張中期電位(MDP)を認めた。同部の心内膜側からの56穴irrigation catheterを用いての通電にてVTは速やかに停止し誘発されなくなった。洞調律中にvoltage mapの作成にて前壁に0.6mV以下の低電位領域を認めた。低電位領域内の瘢痕をつなぎVTの興奮伝播を横切るように通電を追加した(40〜50 W 60 sec)。洞調律中の心内膜側からの高出力の安定した通電でAIV内のILPは徐々に遅延し完全に消失した。以後clinical VTは誘発されなくなった。左室心内外膜側に共通回路を持つ難治性の心室頻拍に対し、多孔性の高出力irrigation catheterを用いることによって、心内膜側からの通電にて心外膜側の共通回路の伝導ブロックを形成し頻拍を根治できた症例を経験したので報告する。(著者抄録)
  • 糖尿病患者に対する心肺運動負荷試験を用いた運動指導の試み
    飛田良, 森野勝太郎, 林秀樹, 岩井宏治, 木下妙子, 川口民郎, 関根理, 卯木聡, 前川聡, 堀江稔
    糖尿病 58(Supplement 1) S.390-390 2015年04月
  • Impact of Updated Diagnostic Criteria for Long QT Syndrome on Clinical Detection of Diseased Patients: Results From a Study of Patients Carrying Gene Mutations
    Kenshi Hayashi, Tetsuo Konno, Noboru Fujino, Hideki Itoh, Yusuke Fujii, Yoko Imi-Hashida, Hayato Tada, Toyonobu Tsuda, Yoshihiro Tanaka, Takekatsu Saito, Hidekazu Ino, Masa aki Kawashiri, Kunio Ohta, Minoru Horie, Masakazu Yamagishi
    JACC: Clinical Electrophysiology 2(3) 279-287 2016年01月
    © 2016 American College of Cardiology Foundation Objectives In this study, we scored patients with long QT syndrome (LQTS) according to the different Schwartz diagnostic criteria from 1993, 2006, and 2011, and to examine the validation of the criteria in relevance to the frequency of LQTS-related gene mutation. Background Although updated diagnostic criteria have been used in clinical settings, few data exist regarding their impact on the diagnosis of LQTS. Methods We used a cohort of 132 patients who presented with prolonged QTc intervals and/or abnormal clinical history in cardiac screening and who underwent exercise stress testing. LQTS scores of ≥3.5 points according to the 2006 and the 2011 criteria were considered to indicate a high probability of LQTS, as opposed to the 4 points used by the 1993 criteria. The 2011 criteria were updated by adding the evaluation of the recovery phase of exercise. Results The 2011 criteria significantly increased the number of high probability patients (n = 62) compared with the 1993 criteria (n = 32; p = 0.0002) or the 2006 criteria (n = 36; p = 0.0014). The percentage of mutation carriers in those with an intermediate score, which was rather high using the 1993 (53%) and 2006 criteria (53%), was greatly reduced with the 2011 criteria (15%, p = 0.0014 vs. the 1993 criteria, and p = 0.0013 vs. the 2006 criteria). Among 54 mutation carriers, the 1993, the 2006, and the 2011 criteria identified a high probability of carriers in 25 patients (46% sensitivity and 91% specificity), 27 patients (50% sensitivity and 88% specificity), and 48 patients (89% sensitivity and 82% specificity), respectively. Conclusions The use of the 2011 criteria will facilitate the diagnosis of LQTS and will decrease the number of false negative results.
  • 肺性P波と心房細動の発生
    林秀樹, 宮本証, 川口民郎, 松本鉄也, 堀江稔
    心電図 35(Supplement 1) 9-1 2015年03月
  • 心電図ST上昇を考える:J波症候群 早期再分極と致死性不整脈:病院症例の検討―J波症候群への考察―
    林秀樹, 内貴乃生, 宮本証, 川口民郎, 杉本喜久, 伊藤誠, XUE Joel Q., 村上義孝, 堀江稔
    心電図 34(4) 368-376 2015年03月
    近年、早期再分極が致死性不整脈発生の新たな心電図所見として注目されている。しかし、早期再分極のすべてが致死性不整脈の原因になっているわけではなく、良性と悪性が存在する。両者の鑑別は極めて重要である。われわれは、病院を受診した症例から構成された心電図データベースを用いて、様々なコホートにおいて早期再分極と致死性不整脈の関係を調べた。早期再分極は、思春期に頻度が高いことが認められ、Brugada症候群・QT短縮症候群・デバイス植込みの症例において、早期再分極と致死性不整脈発生の関係が認められた。今後、早期再分極と治療効果の関連を検討する必要があると考えられた。(著者抄録)
  • 一過性完全房室ブロックを契機に心Fabry病を疑われ遺伝子診断にて診断確定に至った1例
    加藤浩一, 堀江稔, 米田直人, 栗本泰行, 廣吉康秀, 久松恵理子, 山中あすか, 冨澤宗樹, 田中康史, 北川泰生
    滋賀医学 37 159-159 2015年03月
  • 無冠尖からの通電で焼灼し得たATP感受性心房頻拍の1例
    高橋宏明, 藤居祐介, 小澤友哉, 伊藤英樹, 服部哲久, 芦原貴司, 児玉健二, 福沢綾子, 冨田行則, 八木典章, 内貴乃生, 木村紘美, 松本祐一, 中江一郎, 酒井宏, 山本孝, 杉本喜久, 伊藤誠, 堀江稔
    滋賀医学 37 154-154 2015年03月
  • Antiplatelet therapy discontinuation and the risk of serious cardiovascular events after coronary stenting: Observations from the CREDO-Kyoto registry cohort-2
    Hirotoshi Watanabe, Takeshi Morimoto, Masahiro Natsuaki, Yutaka Furukawa, Yoshihisa Nakagawa, Kazushige Kadota, Kyohei Yamaji, Kenji Ando, Satoshi Shizuta, Hiroki Shiomi, Tomohisa Tada, Junichi Tazaki, Yoshihiro Kato, Mamoru Hayano, Mitsuru Abe, Takashi Tamura, Manabu Shirotani, Shinji Miki, Mitsuo Matsuda, Mamoru Takahashi, Katsuhisa Ishii, Masaru Tanaka, Takeshi Aoyama, Osamu Doi, Ryuichi Hattori, Masayuki Kato, Satoru Suwa, Akinori Takizawa, Yoshiki Takatsu, Eiji Shinoda, Hiroshi Eizawa, Teruki Takeda, Jong Dae Lee, Moriaki Inoko, Hisao Ogawa, Shuichi Hamasaki, Minoru Horie, Ryuji Nohara, Hirofumi Kambara, Hisayoshi Fujiwara, Kazuaki Mitsudo, Masakiyo Nobuyoshi, Toru Kita, Adnan Kastrati, Takeshi Kimura
    PLoS ONE 10(4) 2015年04月
    Copyright: © 2015 Watanabe et al. Relation of antiplatelet therapy (APT) discontinuation with the risk of serious cardiovascular events has not been fully addressed yet. This study is aimed to evaluate the risk of ischemic event after APT discontinuation based on long-term APT status of large cohort. In the CREDO-Kyoto Registry Cohort-2 enrolling 15939 consecutive patients undergoing first coronary revascularization, 10470 patients underwent percutaneous coronary intervention either with bare-metal stents (BMS) only (N=5392) or sirolimus-eluting stents (SES) only (N=5078). Proportions of patients taking dual-APT were 67.3% versus 33.4% at 1-year, and 48.7% versus 24.3% at 5-year in the SES and BMS strata, respectively. We evaluated daily APT status (dual-, single- and no-APT) and linked the adverse events to the APT status just 1-day before the events. No-APT as compared with dual- or single-APT was associated with significantly higher risk for stent thrombosis (ST) beyond 1-month after SES implantation (cumulative incidence rates beyond 1-month: 1.23 versus 0.15/0.29, P < 0.001/ P < 0.001), while higher risk of no-APT for ST was evident only until 6-month after BMS implantation (incidence rates between 1- and 6-month: 8.43 versus 0.71/1.20, P < 0.001/ P < 0.001, and cumulative incidence rates beyond 6-month: 0.31 versus 0.11/0.08, P=0.16/ P=0.08). No-APT as compared with dual- or single-APT was also associated with significantly higher risk for spontaneous myocardial infarction (MI) and stroke regardless of the types of stents implanted. Single-APT as compared with dual-APT was not associated with higher risk for serious adverse events, except for the marginally higher risk for ST in the SES stratum. In conclusion, discontinuation of both aspirin and thienopyridines was associated with increased risk for serious cardiovascular events including ST, spontaneous MI and stroke beyond 1-month after coronary stenting.
  • 若年性心房細動患者に同定されたカリウムチャネル変異
    長谷川奏恵, 大野聖子, 芦原貴司, 伊藤英樹, 堀江稔, 牧山武
    滋賀医学 37 96-96 2015年03月
  • 滋賀医科大学アジア疫学研究センターの取り組み : NCD克服のための疫学研究・教育拠点を目指して(特別寄稿)
    三浦 克之, 堀江 稔, 野崎 和彦, 久松 隆史, Abbott Robert D.
    滋賀医科大学看護学ジャーナル 13(1) 8-14 2015年03月
    滋賀医科大学では2013年10月に、新しい総合研究棟(疫学研究拠点)としてアジア疫学研究センターが新築、開所した。本センターは、本学のこれまでの生活習慣病疫学研究の実績を生かし、良好な研究環境による国際共同疫学研究の実施、大規模データベースの管理とバイオバンクによる生体試料保存を行うことを可能にするものである。また、これと時期を同じくして、文部科学省の平成25年度博士課程教育リーディングプログラムが採択され、アジア疫学研究センターを教育基盤とした博士課程教育リーディングプログラム「アジア非感染性疾患(NCD)超克プロジェクト」が開始された。本プログラムでは国内外の産学官の広い分野においてアジア太平洋州のトップリーダーとして活躍するNCD対策の専門家を育成する。
  • Septal concealmentとbundle branch block
    林秀樹, 堀江稔
    滋賀医学 37 160-160 2015年03月
  • Verapamilがelectrical stormに有効であった特発性心室細動の1例
    藤居祐介, 伊藤英樹, 服部哲久, 小澤友哉, 芦原貴司, 児玉健二, 高橋宏明, 福沢綾子, 冨田行則, 八木典章, 松本祐一, 内貴乃生, 木村紘美, 酒井宏, 山本孝, 伊藤誠, 堀江稔
    滋賀医学 37 155-155 2015年03月
  • short‐coupled variant of torsade de pointesの遺伝的背景
    堀本かんな, 伊藤英樹, 藤居祐介, 服部哲久, 小澤友哉, 芦原貴司, 大野聖子, 伊藤誠, 堀江稔
    滋賀医学 37 95-95 2015年03月
  • リハビリテーションを併用し,高度鎖骨下動脈狭窄が改善した大動脈炎症候群の1例
    岩井宏治, 林秀樹, 飛田良, 木下妙子, 川口民郎, 酒井宏, 堀江稔
    心臓 47(2) 180-186 2015年02月
    症例は65歳、女性。右上肢の乏血症状をきたし精査加療目的に入院となった。右橈骨動脈の触知はできず、右上腕での血圧測定は不可であった。造影CTにて右鎖骨下動脈の閉塞を認め、ヒト白血球型抗原-B52が陽性であり、大動脈炎症候群と診断された。副腎皮質ホルモンと抗血小板剤の内服に加え、上肢のリハビリテーションを実施した。負荷制御装置を用いて上肢のアイソキネティック運動(回転数30回/分、15分間)を実施し、また弾性バンドによるレジスタンストレーニングを併用した。運動療法後には、上肢の血行改善を目的にホットパックによる温熱療法も行った。治療9ヵ月後の造影CTと、血管造影検査にて右鎖骨下動脈の血管内径の増大・血流改善を認めた。右鎖骨下動脈狭窄を認めた大動脈症候群症例において、副腎皮質ホルモンの内服に加え長期間のリハビリテーションの継続が、狭窄血管の血行改善に寄与できる可能性が示唆された。(著者抄録)
  • 滋賀医科大学アジア疫学研究センターの取り組み NCD克服のための疫学研究・教育拠点を目指して
    三浦 克之, 堀江 稔, 野崎 和彦, 久松 隆史, Abbott Robert D.
    滋賀医科大学看護学ジャーナル 13(1) 8-14 2015年03月
    滋賀医科大学では2013年10月に、新しい総合研究棟(疫学研究拠点)としてアジア疫学研究センターが新築、開所した。本センターは、本学のこれまでの生活習慣病疫学研究の実績を生かし、良好な研究環境による国際共同疫学研究の実施、大規模データベースの管理とバイオバンクによる生体試料保存を行うことを可能にするものである。また、これと時期を同じくして、文部科学省の平成25年度博士課程教育リーディングプログラムが採択され、アジア疫学研究センターを教育基盤とした博士課程教育リーディングプログラム「アジア非感染性疾患(NCD)超克プロジェクト」が開始された。本プログラムでは国内外の産学官の広い分野においてアジア太平洋州のトップリーダーとして活躍するNCD対策の専門家を育成する。(著者抄録)
  • 心不全患者の栄養状態とエネルギー代謝に関する臨床的検討
    岡崎 量子, 佐々木 雅也, 岩川 裕美, 栗原 美香, 堀江 稔, 浅井 徹, 小松 龍史
    日本病態栄養学会誌 18(Suppl.) S-73 2014年12月
  • 乳児の致死性不整脈と心臓チャネル病の関連について
    加藤 浩一, 牧山 武, Wu Jie, Ding Wei-Guang, 木村 紘美, 内貴 乃生, 大野 聖子, 伊藤 英樹, 中西 敏雄, 松浦 博, 堀江 稔
    福田記念医療技術振興財団情報(27) 19-23 2014年12月
    乳児の致死性不整脈と心臓チャネル病の関連について検討した。1歳未満での致死性不整脈イベントの記録を有する7例を対象とした。5例に心臓イオンチャンネル遺伝子の異常を認め、SCN5A変異が4例、KCNH2の変異が1例であった。機能解析ではSCN5AのN1774D、F1486del、N4066K変異は遅延ナトリウム電流を伴う機能獲得型変異の特徴を示したが、T290fsX53は電流密度が極端に低下する機能喪失型特徴を示した。特に、F1486del変異チャネルに関しては非常に大きい遅延ナトリウム電流が記録され、これに対してIb群のナトリウム遮断薬を使用したところ、著明な遅延電流の抑制が見られた。KCNH2のG628D変異も、電流量が減少する機能喪失型変異の特徴がみられ、WTとの共発現においては弱いdominant negative suppression effectが認められた。
  • Kir3.4変異はKir2.1に対する抑制作用を通してAndersen-Tawil症候群を引き起こす
    古田 充, 穀内 洋介, 中田 智彦, 坂田 宗平, 木村 紘美, 相庭 武司, 吉永 正夫, 大崎 裕亮, 中森 雅之, 伊藤 英樹, 佐藤 貴子, 久保田 智哉, 門田 一繁, 進藤 克郎, 望月 秀樹, 清水 渉, 堀江 稔, 岡村 康司, 大野 欽司, 高橋 正紀
    臨床神経学 54(Suppl.) S30-S30 2014年12月
  • Effect of preinfarction angina pectoris on long-term survival in patients with ST-segment elevation myocardial infarction who underwent primary percutaneous coronary intervention
    Tomohiko Taniguchi, Hiroki Shiomi, Toshiaki Toyota, Takeshi Morimoto, Masaharu Akao, Kenji Nakatsuma, Koh Ono, Takeru Makiyama, Satoshi Shizuta, Yutaka Furukawa, Yoshihisa Nakagawa, Kenji Ando, Kazushige Kadota, Minoru Horie, Takeshi Kimura
    American Journal of Cardiology 114(8) 1179-1186 2014年10月
    ©2014 Elsevier Inc. All rights reserved. The influence of preinfarction angina pectoris (AP) on long-term clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (PCI) remains controversial. In 5,429 patients with acute myocardial infarction (AMI) enrolled in the Coronary Revascularization Demonstrating Outcome Study in Kyoto AMI Registry, the present study population consisted of 3,476 patients with STEMI who underwent primary PCI within 24 hours of symptom onset and in whom the data on preinfarction AP were available. Preinfarction AP defined as AP occurring within 48 hours of hospital arrival was present in 675 patients (19.4%). Patients with preinfarction AP was younger and more often had anterior AMI and longer total ischemic time, whereas they less often had history of heart failure, atrial fibrillation, and shock presentation. The infarct size estimated by peak creatinine phosphokinase was significantly smaller in patients with than in patients without preinfarction AP (median [interquartile range] 2,141 [965 to 3,867] IU/L vs 2,462 [1,257 to 4,495] IU/L, p < 0.001). The cumulative 5-year incidence of death was signi ficantly lower in patients with preinfarction AP (12.4% vs 20.7%, p < 0.001) with median follow-up interval of 1,845 days. After adjusting for confounders, preinfarction AP was independently associated with a lower risk for death (hazard ratio 0.69, 95% confidence interval 0.54 to 0.86, p = 0.001). The lower risk for 5-year mortality in patients with preinfarction AP was consistently observed across subgroups stratified by total ischemic time, initial Thrombolysis In Myocardial Infarction flow grade, hemodynamic status, infarct location, and diabetes mellitus. In conclusion, preinfarction AP was independently associated with lower 5-year mortality in patients with STEMI who underwent primary PCI.
  • βブロッカー療法とカウンセリングが有効であったうつ病合併重症心不全の一例
    酒井宏, 八木典章, 伊藤英樹, 堀江稔
    日本心臓病学会学術集会(Web) 63rd ROMBUNNO.P‐371 (WEB ONLY)-817 2015年09月
  • シタグリプチンとACE阻害薬併用の血行動態とバイオマーカーに及ぼす影響
    蔦本 尚慶, 酒井 宏, 河原 千穂, 内貴 乃生, 和田 厚幸, 堀江 稔
    医学と薬学 71(11) 2103-2110 2014年10月
    目的:高血圧合併の2型糖尿病患者に経口糖尿病薬dipeptidyl peptidase-4(DPP-4)阻害薬が臓器保護作用の可能性と低血糖などの副作用が少ないことから頻用されている。また心臓血管事故の予防や腎保護作用のあるRA系阻害薬(ACE-IまたはARB)が併用されることが多い。最近、ACF-IとDPP-4阻害薬の併用でACE-Iの血圧低下作用が減弱する可能性が報告された。DPP-4阻害薬にRA系阻害薬を併用する際、ACE-IとARBで血圧、心機能、バイオマーカーに及ぼす影響を比較検討した。方法:高血圧合併の2型糖尿病患者(既報)のサブ解析で、ACE-IまたはARBが投与されていた高血圧患者36人に、DPP-4阻害薬シタグリプチン100mg/日を投与し、投与前および12ヵ月後に、血圧測定、心臓超音波検査を施行。同日に採血しHbA1c、血漿BNP濃度、NT-proBNP濃度を測定した。ACE-Iが前投与されていた患者(n=10)とARBが前投与されていた患者(n=26)について比較検討した。結果:ACE-I投与患者において収縮期血圧は126±24mmHgから135±17mmHg(p=0.03)。拡張期血圧は73±11mmHgから78±11mmHg(p=0.02)へと有意に上昇した。BNP濃度は78±95pg/mLから110±129pg/mL(p=0.01)、NT-proBNP濃度は275±321pg/mLから393±506pg/mL(p=0.03)へ有意に増加した。ARB投与患者では収縮期血圧は、129±14mmHgから128±17mmHg、拡張期血圧は73±10mmHgから72.6±10mmHgと変化しなかった。BNP濃度は66±63pg/mLから80±88pg/mL(p=0.19)で変化しなかったが、NT-proBNP濃度は339±468pg/mLから288±458pg/mL(p=0.03)と有意に低下した。左室心筋重量係数はACE-I群で118±30(g/m2)から112±28(g/m2)と変化せず、ARB群で120±33(g/m2)から113±29(g/m2)(p=0.02)に有意に減少した。結語:糖尿病を合併した高血圧患者において、シタグリプチンとRA系阻害薬の併用において、血行動態、心機能、NT-proBNP濃度などの指標から判断してACE-IよりARBとの併用が推奨される。(著者抄録)
  • 【遺伝性不整脈】 遺伝性不整脈の診断とマネージメントのUp-to-Date 3大陸不整脈学会Expert Consensus Statementを中心に
    堀江 稔
    呼吸と循環 62(9) 832-840 2014年09月
  • 運動療法における内臓脂肪の意義 糖尿病での検討
    林 秀樹, 飛田 良, 岩井 宏治, 川口 民郎, 松本 鉄也, 堀江 稔
    日本臨床運動療法学会雑誌 16(1) 72-72 2014年09月
  • Andersen-Tawil症候群iPS細胞に由来する心筋細胞において逆モードNa+/Ca2+交換輸送体阻害薬は不整脈原性基質を抑制する(Reverse-mode Na+/Ca2+ Exchanger Inhibitor Suppresses an Arrhythmogenic Substrate in Andersen-Tawil Syndrome-induced Pluripotent Stem Cell-derived Cardiomyocytes)
    黒田 裕介, 湯浅 慎介, 堀江 稔, 堀米 仁志, 神谷 香一郎, 福田 恵一
    日本心臓病学会学術集会抄録 62回 YIA-3 2014年09月
  • 多様な不整脈の表現型に関連するSCN5Aプロモータの変異体(Variants in SCN5A Promoter Associated with Various Arrhythmia Phenotypes)
    八木原 伸江, 渡部 裕, Barnett Phil, Duboscq-Bidot Laetitia., Thomas Atack C., Yang Ping, 大野 聖子, 長谷川 奏恵, 桑野 良三, Chatel Stephanie, Redon Richard, Schott Jean-Jacques, Probst Vincent, Koopmann Tamara T., Bezzina Connie R., Wilde Arthur A.M., 中野 由紀子, 相庭 武, 宮本 義弘, 鎌倉 史郎, Darbar Dawood, Donahue Brian S., 佐藤 光希, 南野 徹, 遠藤 直人, 清水 渉, 堀江 稔, Roden Dan M., 蒔田 直昌
    日本心臓病学会学術集会抄録 62回 YIA-4 2014年09月
  • 後天性QT延長症候群の遺伝的背景 多施設国際共同研究
    伊藤 英樹, Crotti Lia, 相庭 武司, Denjoy Isabelle, Fressart Veronique, 林 研至, 中島 忠, 大野 聖子, 牧山 武, 山岸 正和, Berthet Myriam, 清水 渉, Guicheney Pascale, Schwartz Peter J., 堀江 稔
    日本心臓病学会学術集会抄録 62回 優O-1 2014年09月
  • Short-coupled Variant of Torsade de Pointesの遺伝学的検討
    藤居 祐介, 伊藤 英樹, 芦原 貴司, 八木 典章, 酒井 宏, 堀江 稔, 中川 義久
    日本心臓病学会学術集会抄録 62回 O-063 2014年09月
  • Wilson病に合併した門脈肺高血圧症の一例
    児玉 健二, 伊藤 英樹, 酒井 宏, 堀江 稔, 田辺 正喜
    日本心臓病学会学術集会抄録 62回 P-190 2014年09月
  • 心肥大の進行が契機となり発見された心ALアミロイドーシスの1例
    八木 典章, 酒井 宏, 冨田 行則, 伊藤 英樹, 山本 孝, 堀江 稔
    日本心臓病学会学術集会抄録 62回 P-420 2014年09月
  • 遺伝性不整脈の診断とマネージメントのUp-to-Date : 3大陸不整脈学会Expert Consensus Statementを中心に (特集 遺伝性不整脈)
    堀江 稔
    呼吸と循環 62(9) 832-840 2014年09月
  • 骨格筋量と運動における仕事との関係
    林秀樹, 松本鉄也, 堀江稔
    日本心臓病学会学術集会(Web) 63rd ROMBUNNO.P‐454 (WEB ONLY)-900 2015年09月
  • 心疾患二次予防における高血圧患者教育の取り組みについて
    八木 典章, 堀江 稔
    Therapeutic Research 35(8) 725-727 2014年08月
    狭心症治療目的で入院中の69歳女を対象として家庭用血圧測定の重要性を教育し、退院後は朝夕に座位・上腕で血圧を3回ずつ測定させ、携帯通信機能付き血圧計とテレメディスンシステムを利用して6ヵ月間管理を行った。このシステムは患者の血圧測定に対する負担を軽減することが可能であり、6ヵ月間ほぼ毎日朝晩に計3回ずつ血圧測定を継続させることができた。また、プロトコールを施行した6ヵ月後には診察室血圧・体重・推定塩分量・脳性ナトリウム利尿ポリペプチド・ヘモグロビンA1c・高比重リポ蛋白/低比重リポ蛋白・左室容積の改善が認められた。
  • QT延長症候群に対する遺伝子検査の有用性
    藤澤 祐介, 林 泰佑, 進藤 考洋, 平田 陽一郎, 犬塚 亮, 清水 信隆, 岡 明, 堀江 稔
    日本小児科学会雑誌 118(7) 1146-1146 2014年07月
  • 不整脈疾患の病態生理 遺伝性不整脈の診断と治療 その病態生理からのアプローチ
    堀江 稔
    日本病態生理学会雑誌 23(2) 28-28 2014年07月
  • 2型糖尿病患者における筋肉量と筋力の関連性 肥満の有無による検討
    飛田 良, 林 秀樹, 森野 勝太郎, 岩井 宏治, 木下 妙子, 川口 民朗, 前川 昭次, 前川 聡, 堀江 稔
    理学療法学 41(大会特別号2) 1278-1278 2014年05月
  • 左室内血栓が急性に出現した拡張型心筋症の一例
    八木 典章, 山路 正之, 伊藤 英樹, 山本 孝, 浅井 徹, 堀江 稔
    滋賀医科大学雑誌 27(1) 9-13 2014年05月
    症例は、49歳男性。健康診断で心拡大を指摘され、近医で高血圧に対して薬物加療が行われていたが、起坐呼吸と下腿浮腫を主訴に当科へ緊急入院となった。入院時から心不全加療としてフロセミドなどの利尿剤を投与し、血栓予防目的でヘパリン10000単位/日とワルファリン2mg投与を開始した。ヘパリンはAPTTで、ワルファリンはPT-INRで効果判定を行い、入院第4病日ではAPTT:29.6秒、PT-INR:1.48であった。同日に施行した心臓超音波検査で左心室内に入院時に認めなかった有茎で浮遊性のある約2cmの血栓を2個認めた。浮遊性の血栓であり、塞栓症の危険性があると判断して、心臓血管外科で左心室内血栓除去術と僧帽弁輪形成術を施行した。術後は薬物加療の強化により経過は良好で第32病日に退院となった。拡張型心筋症の心不全加療は、血流の鬱滞や凝固系亢進の病態から心室内血栓のリスクがあると同時に利尿剤による血液濃縮も重なる可能性があるため、ワルファリンとヘパリンによる抗凝固療法を行う必要性がある。しかしワルファリンの投与初期は、Protein Cの活性化が急激に低下するため、一時的に凝固亢進状態となる。よってAPTTを測定しながら、併用するヘパリンの投与量を調整する必要性が示唆された。また同時に心臓超音波検査で心室内血栓の定期的な評価が必要であることも示唆された。(著者抄録)
  • 左室内血栓が急性に出現した拡張型心筋症の一例
    八木 典章, 山路 正之, 伊藤 英樹, 山本 孝, 浅井 徹, 堀江 稔
    滋賀医科大学雑誌 27(1) 9-13 2014年03月
    A 49-year-old male was admitted to our hospital for therapy of congestive heart failure. He underwent echocardiography, which revealed severe systolic dysfunction of left ventricle as dilated cardiomyopathy, while we were unable to detect thrombus in left ventricle on admission. Coagulation values for D-dimer, congenital antithrombin III and protein C were within the normal range. He was treated with continuous infusion of carperitide and furosemide.Though he immediately started to receive both heparin sodium at a dose of 10,000 units/day and warfarin potassium at a dose of 2 mg/day to avoid thrombus after admission, activated partial thromboplastin (APTT) time and prothrombin time-International normalized ratio (PT-INR) failed to be sufficiently prolonged. A few floating thrombi about 2 centimeters in diameter appeared around the apex of the left ventricle when his left ventricle was assessed by echocardiography after only 3 days .Emergency cardiotomy was performed and all thrombi were successfully removed. This is particularly important because thrombi could fall onto the aortic valve, which could lead to sudden death .
  • 診断に難渋したうっ血性心不全の1例
    児玉 健二, 服部 哲久, 伊藤 英樹, 山本 孝, 伊藤 誠, 堀江 稔, 畔柳 智司, 浅井 徹
    滋賀医学 36 121-121 2014年03月
  • 当院における静脈血栓塞栓症例
    冨田 行則, 八木 典章, 服部 哲久, 内貴 乃生, 木村 紘美, 酒井 宏, 小澤 友哉, 伊藤 英樹, 山本 孝, 伊藤 誠, 堀江 稔
    滋賀医学 36 124-124 2014年03月
  • 致死性不整脈症候群の病態解明に関する研究 臨床・基礎研究(ヒト疾患特異的人工多能性幹(iPS)細胞を用いた解析)
    木村 剛, 北 徹, 堀江 稔, 堀内 久徳, 尾野 亘, 牧山 武, 吉田 善紀
    医科学応用研究財団研究報告 31 447-454 2014年02月
  • A rare KCNE1 polymorphism, D85N, as a genetic modifier of long QT syndrome
    Kanae Hasegawa, Seiko Ohno, Hideki Itoh, Takeru Makiyama, Takeshi Aiba, Yasutaka Nakano, Wataru Shimizu, Hiroshi Matsuura, Naomasa Makita, Minoru Horie
    Journal of Arrhythmia 30 161-166 2014年01月
    © 2013 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved. Background: The gene KCNE1 encodes the β-subunit of cardiac voltage-gated K + channels and causes long QT syndrome (LQTS). LQTS is characterized by the prolongation of QT interval and lethal arrhythmias such as torsade de pointes (TdP). A KCNE1 polymorphism, D85N, has been shown to modify the phenotype of LQTS through a loss-of-function effect on both KCNQ1 and KCNH2 channels when co-expressed and reconstituted in a heterologous expression system. Methods: A screening for the D85N polymorphism was performed in 355 LQTS families with mutations in KCNQ1, KCNH2, or SCN5A. Among the probands who had a heterozygous status with the polymorphism, we focused on a family with a KCNH2 mutation (E58K), a N-terminal missense mutation, and examined the clinical significance of this polymorphism. We also conducted biophysical assays to analyze the effect of the polymorphism in mammalian cells. Results: In 355 probands, we found 14 probands (3.9%) who had a heterozygous compound status with the D85N polymorphism. In the family with a KCNE1-D85N polymorphism and a KCNH2-E58K mutation, the proband and her daughter carried both the KCNH2 mutation and the KCNE1-D85N polymorphism. They experienced repetitive syncope and TdP. Two sons of the proband had either KCNH2-E58K mutation or KCNE1-D85N, but were asymptomatic. Biophysical assays of KCNE1-D85N with KCNH2-E58K variants produced a larger reduction in the reconstituted I Kr currents compared to co-expression with wild-type KCNE1. Conclusions: The KCNE1-D85N polymorphism modified the clinical features of LQTS patients.
  • Gain-of-function KCNH2 mutations in patients with Brugada syndrome
    Qi Wang, Seiko Ohno, Wei Guang Ding, Megumi Fukuyama, Akashi Miyamoto, Hideki Itoh, Takeru Makiyama, Jie Wu, Jiayu Bai, Kanae Hasegawa, Tetsuji Shinohara, Naohiko Takahashi, Akihiko Shimizu, Hiroshi Matsuura, Minoru Horie
    Journal of Cardiovascular Electrophysiology 25(5) 522-530 2014年01月
    Novel KCNH2 Mutations in Brugada Syndrome Background Brugada syndrome (BrS) is an inherited disease characterized by right precordial ST segment elevation on electrocardiograms (ECGs) that predisposes patients to sudden cardiac death as a result of polymorphic ventricular tachyarrhythmia or ventricular fibrillation (VF). In BrS patients, except for SCN5A, mutations in other responsible genes are poorly elucidated. Methods and Results We identified 4 KCNH2 mutations, T152I, R164C, W927G, and R1135H, in 236 consecutive probands with BrS or Brugada-like ECG. Three of these mutation carriers showed QTc intervals shorter than 360 milliseconds and 1 experienced VF. We performed patch-clamp analyses on I Kr reconstituted with the KCNH2 mutations in Chinese hamster ovary cells and compared the phenotypes of the patients with different genotypes. Three mutations, R164C, W927G, and R1135H, increased I Kr densities. Three mutations, T152I, R164C, and W927G, caused a negative shift in voltage-dependent activation curves. Only the R1135H mutant channel prolonged the deactivation time constants. We also identified 20 SCN5A and 5 CACNA1C mutation carriers in our cohort. Comparison of probands' phenotypes with 3 different genotypes revealed that KCNH2 mutation carriers showed shorter QTc intervals and SCN5A mutation carriers had longer QRS durations. Conclusions All KCNH2 mutations that we identified in probands with BrS exerted gain-of-function effects on I Kr channels, which may partially explain the ECG findings in our patients. © 2014 Wiley Periodicals, Inc.
  • Executive summary: HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes
    Silvia G. Priori, Silvia G. Priori, Silvia G. Priori, Arthur A. Wilde, Arthur A. Wilde, Minoru Horie, Yongkeun Cho, Elijah R. Behr, Charles Berul, Nico Blom, Josep Brugada, Chern En Chiang, Heikki Huikuri, Prince Kannankeril, Andrew Krahn, Antoine Leenhardt, Arthur Moss, Peter J. Schwartz, Wataru Shimizu, Gordon Tomaselli, Cynthia Tracy
    Journal of Arrhythmia 30 29-47 2014年01月
  • A novel KCNQ1 missense mutation identified in a patient with juvenile-onset atrial fibrillation causes constitutively open IKs channels
    Kanae Hasegawa, Kanae Hasegawa, Seiko Ohno, Takashi Ashihara, Hideki Itoh, Wei Guang Ding, Futoshi Toyoda, Takeru Makiyama, Hisaaki Aoki, Yoshihide Nakamura, Brian P. Delisle, Hiroshi Matsuura, Minoru Horie
    Heart Rhythm 11(1) 67-75 2014年01月
    Background Atrial fibrillation (AF) is one of the most common cardiac arrhythmias. In some patients, the disease is inheritable; however, hereditary aspects of AF remain not fully elucidated. Objective The purpose of this study was to identify genetic backgrounds that contribute to juvenile-onset AF and to define the mechanism. Methods In 30 consecutive juvenile-onset AF patients (onset age < 50 years), we screened AF-related genes (KCNQ1, KCNH2, KCNE1-3, KCNE5, KCNJ2, SCN5A). We analyzed the function of mutant channels using whole-cell patch-clamp techniques and computer simulations. Results Among the juvenile-onset AF patients, we identified three mutations (10%): SCN5A-M1875T, KCNJ2-M301K, and KCNQ1-G229D. Because KCNQ1 variant (G229D) identified in a 16-year-old boy was novel, we focused on the proband. The G229D-I Ks was found to induce a large instantaneous activating component without deactivation after repolarization to-50 mV. In addition, wild-type (WT)/G229D-I Ks (WT and mutant coexpression) displayed both instantaneous and time-dependent activating currents. Compared to WT-I Ks , the tail current densities in WT/G229D-I Ks were larger at test potentials between-130 and-40 mV but smaller at test potentials between 20 and 50 mV. Moreover, WT/G229D-I Ks resulted in a negative voltage shift for current activation (-35.2 mV) and slower deactivation. WT/G229D-I Ks conducted a large outward current induced by an atrial action potential waveform, and computer simulation incorporating the WT/G229D-I Ks results revealed that the mutation shortened atrial but not ventricular action potential. Conclusion A novel KCNQ1-G229D mutation identified in a juvenile-onset AF patient altered the I Ks activity and kinetics, thereby increasing the arrhythmogenicity to AF. © 2014 Heart Rhythm Society. All rights reserved.
  • Late adverse events after implantation of sirolimus-eluting stent and bare-metal stent long-term (5-7 years) follow-up of the coronary revascularization demonstrating outcome study-kyoto registry cohort-2
    Masahiro Natsuaki, Takeshi Morimoto, Takeshi Morimoto, Yutaka Furukawa, Yutaka Furukawa, Yoshihisa Nakagawa, Yoshihisa Nakagawa, Kazushige Kadota, Kazushige Kadota, Kyohei Yamaji, Kyohei Yamaji, Kenji Ando, Kenji Ando, Satoshi Shizuta, Hiroki Shiomi, Tomohisa Tada, Junichi Tazaki, Yoshihiro Kato, Mamoru Hayano, Mitsuru Abe, Mitsuru Abe, Takashi Tamura, Takashi Tamura, Manabu Shirotani, Manabu Shirotani, Shinji Miki, Shinji Miki, Mitsuo Matsuda, Mitsuo Matsuda, Mamoru Takahashi, Mamoru Takahashi, Katsuhisa Ishii, Katsuhisa Ishii, Masaru Tanaka, Masaru Tanaka, Takeshi Aoyama, Takeshi Aoyama, Osamu Doi, Osamu Doi, Ryuichi Hattori, Ryuichi Hattori, Masayuki Kato, Masayuki Kato, Satoru Suwa, Satoru Suwa, Akinori Takizawa, Akinori Takizawa, Yoshiki Takatsu, Yoshiki Takatsu, Yoshiki Takatsu, Eiji Shinoda, Eiji Shinoda, Eiji Shinoda, Hiroshi Eizawa, Hiroshi Eizawa, Teruki Takeda, Teruki Takeda, Jong Dae Lee, Jong Dae Lee, Moriaki Inoko, Moriaki Inoko, Hisao Ogawa, Hisao Ogawa, Shuichi Hamasaki, Shuichi Hamasaki, Minoru Horie, Minoru Horie, Ryuji Nohara, Ryuji Nohara, Hirofumi Kambara, Hirofumi Kambara, Hisayoshi Fujiwara, Hisayoshi Fujiwara, Kazuaki Mitsudo, Kazuaki Mitsudo, Masakiyo Nobuyoshi, Masakiyo Nobuyoshi, Toru Kita, Toru Kita, Takeshi Kimura
    Circulation: Cardiovascular Interventions 7 168-179 2014年01月
    Background-Late adverse events such as very late stent thrombosis (VLST) or late target-lesion revascularization (TLR) after first-generation sirolimus-eluting stents (SES) implantation have not been yet fully characterized at long term in comparison with those after bare-metal stent (BMS) implantation. Methods and Results-Among 13 058 consecutive patients undergoing first percutaneous coronary intervention in the Coronary REvascularization Demonstrating Outcome study-Kyoto registry Cohort-2, 5078 patients were treated with SES only, and 5392 patients were treated with BMS only. During 7-year follow-up, VLST and late TLR beyond 1 year after SES implantation occurred constantly and without attenuation at 0.24% per year and at 2.0% per year, respectively. Cumulative 7-year incidence of VLST was significantly higher in the SES group than that in the BMS group (1.43% versus 0.68%, P < 0.0001). However, there was no excess of all-cause death beyond 1 year in the SES group as compared with that in the BMS group (20.8% versus 19.6%, P=0.91). Cumulative incidences of late TLR (both overall and clinically driven) were also significantly higher in the SES group than in the BMS group (12.0% versus 4.1%, P < 0.0001 and 8.5% versus 2.6%, P < 0.0001, respectively), leading to late catch-up of the SES group to the BMS group regarding TLR through the entire 7-year follow-up (18.8% versus 25.2%, and 10.6% versus 10.2%, respectively). Clinical presentation as acute coronary syndrome was more common at the time of late SES TLR compared with early SES TLR (21.2% and 10.0%). Conclusions-Late catch-up phenomenon regarding stent thrombosis and TLR was significantly more pronounced with SES than that with BMS. This limitation should remain the target for improvements of DES technology. © 2014 American Heart Association, Inc.
  • Nonsense-mediated mRNA decay due to a CACNA1C splicing mutation in a patient with Brugada syndrome
    Megumi Fukuyama, Seiko Ohno, Qi Wang, Takeshi Shirayama, Hideki Itoh, Minoru Horie
    Heart Rhythm 11(4) 629-634 2014年01月
    Background: Brugada syndrome (BrS) is an inherited cardiac arrhythmia associated with sudden death due to ventricular fibrillation. Mutations in genes related to the cardiac L-type calcium channel have been reported to be causative of BrS. Generally, the messenger RNA (mRNA) that contains a nonsense mutation is rapidly degraded via its decay pathway, which is known as nonsense-mediated mRNA decay (NMD). Previously, we reported a male patient with BrS who carried c.1896G > A (the first nucleotide of CACNA1C exon 14), which caused a synonymous mutation, p.R632R. Objective: To examine how the synonymous CACNA1C mutation p.R632R produces the phenotype of BrS, with a special emphasis on the splicing error and NMD processes. Methods: We extracted mRNA from leukocytes of the proband and his 2 children and performed reverse transcription polymerase chain reaction. Complementary DNAs were checked by using direct sequencing and quantitative analysis. Results: The subsequent sequence electropherogram of the complementary DNAs did not show the substitution of the nucleotide identified in the genomic DNA of the proband. In the mRNA quantification analysis, we confirmed that reduction in the CACNA1C expression level was suspected to be caused by NMD. Conclusions: Mutant mRNA with a c.1896G > A substitution may be diminished by NMD, and the resultant decrease in CACNA1C message leads to a novel mechanism for inducing BrS that is distinct from that reported previously. © 2014 Heart Rhythm Society. All rights reserved.
  • Diagnosis and management of patients with inherited primary arrhythmia syndromes
    Minoru Horie
    Respiration and Circulation 62 832-840 2014年01月
  • Genetic characteristics of children and adolescents with long-QT syndrome diagnosed by school-based electrocardiographic screening programs
    Masao Yoshinaga, Yu Kucho, Jav Sarantuya, Yumiko Ninomiya, Hitoshi Horigome, Hiroya Ushinohama, Wataru Shimizu, Minoru Horie
    Circulation: Arrhythmia and Electrophysiology 7(1) 107-112 2014年01月
    Background-A school-based electrocardiographic screening program has been developed in Japan. However, few data are available on the genetic characteristics of pediatric patients with long-QT syndrome who were diagnosed by this program. Methods and Results-A total of 117 unrelated probands aged =18 years were the subjects who were referred to our centers for genetic testing. Of these, 69 subjects diagnosed by the program formed the screened group. A total of 48 subjects were included in the clinical group and were diagnosed with long-QT syndrome-related symptoms, familial study, or by chance. Mutations were classified as radical, of high probability of pathogenicity, or of uncertain significance. Two subjects in the clinical group died. Genotypes were identified in 50 (72%) and 23 (48%) of subjects in the screened and clinical groups, respectively. Of the KCNQ1 or KCNH2 mutations, 31 of 33 (94%) in the screened group and 15 of 16 (94%) in the clinical group were radical and of high probability of pathogenicity. Prevalence of symptoms before (9/69 versus 31/48; P < 0.0001) and after (12/69 versus 17/48; P=0.03) diagnosis was significantly lower in the screened group when compared with that in the clinical group although the QTc values, family history of long-QT syndrome, sudden death, and follow-up periods were not different between the groups. Conclusions-These data suggest that the screening program may be effective for early diagnosis of long-QT syndrome that may allow intervention before symptoms. In addition, screened patients should have follow-up equivalent to clinically identified patients. © 2013 American Heart Association, Inc.
  • HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes
    Silvia G. Priori, Silvia G. Priori, Silvia G. Priori, Arthur A. Wilde, Arthur A. Wilde, Minoru Horie, Yongkeun Cho, Elijah R. Behr, Charles Berul, Nico Blom, Josep Brugada, Chern En Chiang, Heikki Huikuri, Prince Kannankeril, Andrew Krahn, Antoine Leenhardt, Arthur Moss, Peter J. Schwartz, Wataru Shimizu, Gordon Tomaselli, Cynthia Tracy
    Journal of Arrhythmia 30(1) 1-28 2014年01月
  • Cardiac channelopathies associated with infantile fatal ventricular arrhythmias: From the cradle to the bench
    Koichi Kato, Takeru Makiyama, Jie Wu, Jie Wu, Wei Guang Ding, Hiromi Kimura, Nobu Naiki, Seiko Ohno, Hideki Itoh, Toshio Nakanishi, Hiroshi Matsuura, Minoru Horie
    Journal of Cardiovascular Electrophysiology 25(1) 66-73 2014年01月
    Channelopathies in Infantile Arrhythmias Background Fatal ventricular arrhythmias in the early period of life have been associated with cardiac channelopathies for decades, and postmortem analyses in SIDS victims have provided evidence of this association. However, the prevalence and functional properties of cardiac ion channel mutations in infantile fatal arrhythmia cases are not clear. Methods and Results Seven infants with potentially lethal arrhythmias at age < 1 year (5 males, age of onset 44.1 ± 72.1 days) were genetically analyzed for KCNQ1, KCNH2, KCNE1-5, KCNJ2, SCN5A, GJA5, and CALM1 by using denaturing high-performance liquid chromatography and direct sequencing. Whole-cell currents of wildtype and mutant channels were recorded and analyzed in Chinese hamster ovary cells transfected with SCN5A and KCNH2 cDNA. In 5 of 7 patients, we identified 4 mutations (p.N1774D, p.T290fsX53, p.F1486del and p.N406K) in SCN5A, and 1 mutation (p.G628D) in KCNH2. N1774D, F1486del, and N406K in SCN5A displayed tetrodotoxin-sensitive persistent late Na + currents. By contrast, SCN5A-T290fsX53 was nonfunctional. KCNH2-G628D exhibited loss of channel function. Conclusion Genetic screening of 7 patients was used to demonstrate the high prevalence of cardiac channelopathies. Functional assays revealed both gain and loss of channel function in SCN5A mutations, as well as loss of function associated with the KCNH2 mutation. © 2014 Wiley Periodicals, Inc.
  • Successful control of life-threatening polymorphic ventricular tachycardia by radiofrequency catheter ablation in an infant
    Yuriko Abe, Naokata Sumitomo, Hiromi Okuma, Takahiro Nakamura, Junji Fukuhara, Rie Ichikawa, Masaharu Matsumura, Michio Miyashita, Hiroshi Kamiyama, Mamoru Ayusawa, Mamie Watanabe, Kunitaka Joo, Naomasa Makita, Minoru Horie
    Heart and Vessels 29(3) 422-426 2014年01月
    We present a case of a 9-month-old girl in whom malignant polymorphic ventricular tachycardia (VT) was successfully controlled by radiofrequency catheter ablation under guidance with a three-dimensional mapping system. The VTs originated from the left ventricular lateral wall, left ventricular anterior wall, and left ventricular apex. At least six types of VTs were documented during the electrophysiology study. All VTs were successfully controlled after two sessions of radiofrequency catheter ablation, and she was discharged from our hospital on propranolol, mexiletine, flecainide, and aprindine. © Springer 2013.
  • Exon 3 deletion of RYR2 encoding cardiac ryanodine receptor is associated with left ventricular non-compaction
    Seiko Ohno, Masato Omura, Mihoko Kawamura, Hiromi Kimura, Hideki Itoh, Takeru Makiyama, Hiroya Ushinohama, Naomasa Makita, Minoru Horie
    Europace 16(11) 1646-1654 2014年01月
    © 2014 Published on behalf of the European Society of Cardiology. All rights reserved. Methods and results Our cohort consisted of 24 CPVT probands. Polymerase chain reaction (PCR)-based conventional genetic analysis did not identify any mutations in coding exons of RYR2 in these probands. They were screened using multiplex ligation-dependent probe amplification (MLPA). In probands identified with RYR2 exon 3 deletion, the precise location of the deletion was identified by quantitative PCR and direct sequencing methods. We identified two CPVT probands from unrelated families who harboured a large deletion including exon 3. The probands were 9- and 17-year-old girls. Both probands had a history of syncope related to emotional stress or exercise, exhibited bradycardia, and were diagnosed with left ventricular non-compaction (LVNC). We examined 10 family members and identified six more RYR2 exon 3 deletion carriers. In total, there were eight carriers, of which seven were diagnosed with LVNC (87.5%). Two carriers under the age of 4 years remained asymptomatic, although they were diagnosed with LVNC. Using quantitative PCR and direct sequencing, we confirmed that the deletions were 1.1 and 37.7 kb in length. Conclusion RYR2 exon 3 deletion is frequently associated with LVNC. Therefore, detection of the deletion offers a new modality for predicting the prognosis of patients with LVNC with ventricular/atrial arrhythmias, particularly in children. Aims Ryanodine receptor gene (RYR2) mutations are well known to cause catecholaminergic polymorphic ventricular tachycardia (CPVT). Recently, RYR2 exon 3 deletion has been identified in patients with dilated cardiomyopathy (DCM) and/or CPVT. This study aimed to screen for the RYR2 exon 3 deletion in CPVT probands, characterize its clinical pathology, and confirm the genomic rearrangement.
  • Clinical usefulness of a novel program “Heart Function View” for evaluating cardiac function from gated myocardial perfusion SPECT
    Ichiro Nakae, Hideki Hayashi, Tetsuya Matsumoto, Kenichi Mitsunami, Minoru Horie
    Annals of Nuclear Medicine 28(8) 812-823 2014年01月
    © 2014, The Japanese Society of Nuclear Medicine. Objective: To investigate clinical usefulness of a novel program “Heart Function View (HFV)” for evaluating left ventricular (LV) function from myocardial perfusion SPECT (MPS), we compared LV functional parameters (F(x)) calculated by HFV with those obtained by the other similar programs QGS and cardioGRAF or by ultrasound echocardiography (UCG) and examined their correlations with clinical markers of heart failure: plasma BNP concentrations (BNPs) and exercise capacity. Methods: Studied patients (n = 60) underwent technetium-99m tetrofosmin quantitative gated MPS including treadmill exercise for examining heart disease. Myocardial stress images were acquired 30 min after the first tracer injection during maximal exercise. Three hours later, the second tracer was injected, and resting images were acquired. LV systolic F(x) [ejection fraction (EF), peak ejection rate (PER)] and diastolic F(x) [first third filling fraction (1/3FF), first third filling rate (1/3FR), peak filling rate (PFR), time to PFR (TPF)] were analyzed, and phase standard deviation (SD) and histogram bandwidth were obtained by phase analysis. Results: LV end-diastolic volume (EDV), end-systolic volume (ESV) and EF obtained from HFV were well correlated with those from QGS, cardioGRAF and UCG. A diastolic parameter Doppler E/e′ from UCG was significantly with PFR from HFV. There were good correlations between LVEDV, LVESV, LVEF, PER, PFR, 1/3FR, TPF and 1/3FF from HFV and those from cardioGRAF. LVEF, PER, 1/3FR, and PFR were significantly correlated with plasma BNP concentrations. In patients with non-ischemic heart disease (n = 42), phase SD and histogram bandwidth were correlated negatively with exercise capacity or PFR. Conclusions: HFV-derived LVF(x) are correlated with LVF(x) from the other programs or UCG, or with the clinical markers of heart failure and are thus useful in the functional assessment for patients with heart disease.
  • Executive Summary: HRS/EHRA/APHRS Expert Consensus Statement on the Diagnosis and Management of Patients with Inherited Primary Arrhythmia Syndromes
    Silvia G. Priori, Arthur A. Wilde, Minoru Horie, Yongkeun Cho, Elijah R. Behr, Charles Berul, Nico Blom, Josep Brugada, Chern En Chiang, Heikki Huikuri, Prince Kannankeril, Andrew Krahn, Antoine Leenhardt, Arthur Moss, Peter J. Schwartz, Wataru Shimizu, Gordon Tomaselli, Cynthia Tracy
    Heart Rhythm 10(12) 85-103 2013年12月
  • Effect of flecainide on T-wave alternans in andersen-tawil syndrome
    Hideki Hayashi, Tamiro Kawaguchi, Minoru Horie
    Annals of Noninvasive Electrocardiology 19(4) 383-386 2014年01月
  • HRS/EHRA/APHRS Expert Consensus Statement on the Diagnosis and Management of Patients with Inherited Primary Arrhythmia Syndromes: Document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013.
    Silvia G. Priori, Arthur A. Wilde, Minoru Horie, Yongkeun Cho, Elijah R. Behr, Charles Berul, Nico Blom, Josep Brugada, Chern En Chiang, Heikki Huikuri, Prince Kannankeril, Andrew Krahn, Antoine Leenhardt, Arthur Moss, Peter J. Schwartz, Wataru Shimizu, Gordon Tomaselli, Cynthia Tracy, Cynthia Tracy
    Heart Rhythm 10(12) 1932-1963 2013年12月
  • Naチャネルのスプライシング異常が筋強直性ジストロフィーの心臓伝導障害に関与する
    穀内 洋介, 紀 嘉浩, Li Moy, 伊藤 英樹, 中森 雅之, 木村 卓, 松村 剛, 藤村 晴俊, 貫名 信行, 堀江 稔, 石浦 章一, Swanson Maurice, 望月 秀樹, 佐古田 三郎, 井本 敬二, Charlet-Berguerand Nicolas, 高橋 正紀
    臨床神経学 53(12) 1412-1412 2013年12月
  • 不整脈を伴う低カリウム性周期性四肢麻痺の新規原因遺伝子同定とチャネル機能解析
    高橋 正紀, 穀内 洋介, 中田 智彦, 坂田 宗平, 大崎 裕亮, 中森 雅之, 木村 紘美, 伊藤 英樹, 久保田 智哉, 進藤 克郎, 望月 秀樹, 堀江 稔, 岡村 康司, 大野 欽司
    臨床神経学 53(12) 1470-1470 2013年12月
  • Pharmacological correction of long QT-linked mutations in KCNH2 (hERG) increases the trafficking of Kv11.1 channels stored in the transitional endoplasmic reticulum
    Jennifer L. Smith, Allison R. Reloj, Parvathi S. Nataraj, Daniel C. Bartos, Elizabeth A. Schroder, Arthur J. Moss, Seiko Ohno, Minoru Horie, Corey L. Anderson, Craig T. January, Brian P. Delisle
    American Journal of Physiology - Cell Physiology 305(5,Pt.1) 919-930 2013年11月
    KCNH2 encodes Kv11.1 and underlies the rapidly activating delayed rectifier K + current (I Kr ) in the heart. Loss-of-function KCNH2 mutations cause the type 2 long QT syndrome (LQT2), and most LQT2-linked missense mutations inhibit the trafficking of Kv11.1 channels. Drugs that bind to Kv11.1 and block I Kr (e.g., E-4031) can act as pharmacological chaperones to increase the trafficking and functional expression for most LQT2 channels (pharmacological correction). We previously showed that LQT2 channels are selectively stored in a microtubuledependent compartment within the endoplasmic reticulum (ER). We tested the hypothesis that pharmacological correction promotes the trafficking of LQT2 channels stored in this compartment. Confocal analyses of cells expressing the trafficking-deficient LQT2 channel G601S showed that the microtubule-dependent ER compartment is the transitional ER. Experiments with E-4031 and the protein synthesis inhibitor cycloheximide suggested that pharmacological correction promotes the trafficking of G601S stored in this compartment. Treating cells in E-4031 or ranolazine (a drug that blocks I Kr and has a short half-life) for 30 min was sufficient to cause pharmacological correction. Moreover, the increased functional expression of G601S persisted 4-5 h after drug washout. Coexpression studies with a dominant- negative form of Rab11B, a small GTPase that regulates Kv11.1 trafficking, prevented the pharmacological correction of G601S trafficking from the transitional ER. These data suggest that pharmacological correction quickly increases the trafficking of LQT2 channels stored in the transitional ER via a Rab11B-dependent pathway, and we conclude that the pharmacological chaperone activity of drugs like ranolazine might have therapeutic potential. © 2013 the American Physiological Society.
  • Sudden cardiac arrest recorded during Holter monitoring: Prevalence, antecedent electrical events, and outcomes
    Eiichi Watanabe, Teruhisa Tanabe, Motohisa Osaka, Akiko Chishaki, Bonpei Takase, Shinichi Niwano, Ichiro Watanabe, Kaoru Sugi, Takao Katoh, Kan Takayanagi, Koushi Mawatari, Minoru Horie, Ken Okumura, Hiroshi Inoue, Hirotsugu Atarashi, Iwao Yamaguchi, Susumu Nagasawa, Kazuo Moroe, Itsuo Kodama, Tsuneaki Sugimoto, Yoshifusa Aizawa
    Heart Rhythm 11(8) 1418-1425 2014年01月
    Background Causative arrhythmias of sudden cardiac arrest (SCA) are changing in this age of improved coronary care. Objective The purpose of this study was to examine the frequency of terminal arrhythmias and the electrical events prior to SCA. Methods We analyzed 24-hour Holter recordings of 132 patients enrolled from 41 institutions who either died (n = 88) or had an aborted death (n = 44). The Holter recordings were obtained for diagnosing and evaluating diseases and arrhythmias in those without any episodes suggestive of SCA. Results In 97 patients (73%), SCA was associated with ventricular tachyarrhythmias and in 35 (27%) with bradyarrhythmias. The bradyarrhythmia- related SCA patients were older than those with a tachyarrhythmia-related SCA (70 ± 13 years vs 58 ± 19 years, P < .001). The most common arrhythmia for a tachyarrhythmia-related SCA was ventricular tachycardia degenerating to ventricular fibrillation (45%). The bradyarrhythmia-related SCA was caused by asystole (74%) or AV block (26%). Spontaneous conversion was observed in 37 patients (38%) with ventricular tachyarrhythmias. Of those, 62% of the patients experienced symptoms including syncope, chest pain, or convulsion. Multivariate logistic analysis revealed that independent predictors of mortality for tachyarrhythmia-related SCAs were advanced age (odds ratio 1.04, 95% confidence interval 1.02-1.08) and ST elevation within the hour before SCA (odds ratio 3.54, 95% confidence interval 1.07-13.5). In contrast, the presence of preceding torsades de pointes was associated with spontaneous conversion (odds ratio 0.20, 95% confidence interval 0.05-0.66). Conclusion The most frequent cause of SCA remains ventricular tachyarrhythmias. Advanced age and ST elevation before SCA are risk factors for mortality in tachyarrhythmia-related SCAs. © 2014 Heart Rhythm Society. All right sreserved.
  • Erratum: Common variants at SCN5A-SCN10A and HEY2 are associated with Brugada syndrome, a rare disease with high risk of sudden cardiac death (Nature Genetics (2013) 45 (1044-1049))
    Connie R. Bezzina, Julien Barc, Yuka Mizusawa, Carol Ann Remme, Jean Baptiste Gourraud, Floriane Simonet, Arie O. Verkerk, Peter J. Schwartz, Lia Crotti, Federica Dagradi, Pascale Guicheney, Véronique Fressart, Antoine Leenhardt, Charles Antzelevitch, Susan Bartkowiak, Eric Schulze-Bahr, Sven Zumhagen, Elijah R. Behr, Rachel Bastiaenen, Jacob Tfelt-Hansen, Morten Salling Olesen, Stefan Kääb, Britt M. Beckmann, Peter Weeke, Hiroshi Watanabe, Naoto Endo, Tohru Minamino, Minoru Horie, Seiko Ohno, Kanae Hasegawa, Naomasa Makita, Akihiko Nogami, Wataru Shimizu, Takeshi Aiba, Philippe Froguel, Beverley Balkau, Olivier Lantieri, Margherita Torchio, Cornelia Wiese, David Weber, Rianne Wolswinkel, Ruben Coronel, Bas J. Boukens, Stéphane Bézieau, Eric Charpentier, Stéphanie Chatel, Aurore Despres, Françoise Gros, Florence Kyndt, Simon Lecointe, Pierre Lindenbaum, Vincent Portero, Jade Violleau, Manfred Gessler, Hanno L. Tan, Dan M. Roden, Vincent M. Christoffels, Hervé Le Marec, Arthur A. Wilde, Vincent Probst, Jean Jacques Schott, Christian Dina, Richard Redon
    Nature Genetics 45(11) 1409 2013年11月
  • Clinical significance of lung iodine-123 metaiodobenzylguanidine uptake assessment in Parkinson's and heart diseases
    Ichiro Nakae, Hideki Hayashi, Kenichi Mitsunami, Minoru Horie
    Annals of Nuclear Medicine 27(8) 737-747 2013年10月
    Objective: Decreased heart iodine-123 metaiodobenzylguanidine ( 123 I-MIBG) uptake [heart-to-mediastinum count ratio (H/M)] is reported in heart disease (HD) or Lewy body disease (LBD). When LBD is merged, therefore, information regarding HD severity may be ambiguous. We aimed to examine whether lung 123 I-MIBG uptake [lung-to-mediastinum count ratio (L/M)] assessment might be useful for differentiating two clinical conditions of HD and LBD, and to investigate whether L/M could reflect the grade of left ventricular (LV) dysfunction. Methods: Three groups were examined: LBD (patient group with Parkinson's disease or dementia with Lewy bodies, n = 33), PS (group with other Parkinsonian syndromes, n = 20) and HD (group with heart disease). HD consisted of 4 subgroups: HD(I) [H/M( < 2.30)-matched group with LBD, n = 34), HD(II) [H/M(≥2.30)-matched group with PS, n = 33], HD(III) [group for functional analysis, LV ejection fraction, first-third and peak filling rates (1/3FR and PFR) and time to PFR were calculated using gated SPECT, n = 35] and HD(IV) (group for examining cardiac prognosis, follow-up period of 1283 ± 506 days, n = 54). Using Doppler echocardiography, a diastolic parameter E/e′ and pulmonary artery pressure (ePAP) were estimated. Results: H/Ms did not differ between HD(I) and LBD, or between PS and HD(II). However, L/Ms were increased in the order of LBD, PS, HD(II) and HD(I) groups. In combined LBD, PS, HD(I) and HD(II), L/Ms correlated positively with a diastolic parameter E/e′. L/Ms correlated with ePAP, while H/Ms did not. H/Ms correlated with a systolic parameter EF (r = 0.56) and diastolic parameters 1/3FR (r = 0.51) and PFR (r = 0.51), and L/Ms correlated with diastolic parameters 1/3FR (r = -0.36) and PFR (r = -0.36) but not with EF in HD(III). Kaplan-Meier analysis showed earlier cardiac death in patients with decreased H/Ms, but not in patients with increased L/Ms in HD(IV). Conclusions: Our study suggest that increased lung 123 I-MIBG uptake is useful as a reference marker for differentiating two clinical conditions of HD and LBD, and can reflect the degree of LV diastolic dysfunction. Elevated ePAP caused by LV diastolic dysfunction may be involved in the mechanism(s) of increased lung uptake. © 2013 The Japanese Society of Nuclear Medicine.
  • Executive summary: HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes.
    Silvia G. Priori, Arthur A. Wilde, Minoru Horie, Yongkeun Cho, Elijah R. Behr, Charles Berul, Nico Blom, Josep Brugada, Chern En Chiang, Heikki Huikuri, Prince Kannankeril, Andrew Krahn, Antoine Leenhardt, Arthur Moss, Peter J. Schwartz, Wataru Shimizu, Gordon Tomaselli, Cynthia Tracy, Document Reviewers, Michael Ackerman, Bernard Belhassen, N. A.Mark Estes, Diane Fatkin, Jonathan Kalman, Elizabeth Kaufman, Paulus Kirchhof, Eric Schulze-Bahr, Christian Wolpert, Jitendra Vohra, Marwan Refaat, Susan P. Etheridge, Robert M. Campbell, Edward T. Martin, Swee Chye Quek, Heart Rhythm Society, European Heart Rhythm Association, Asia Pacific Heart Rhythm Society
    Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology 15 1389-1406 2013年10月
  • Electrical storm in idiopathic ventricular fibrillation is associated with early repolarization
    Yoshifusa Aizawa, Yoshifusa Aizawa, Masaomi Chinushi, Kanae Hasegawa, Nobu Naiki, Minoru Horie, Yoshiaki Kaneko, Masahiko Kurabayashi, Shogo Ito, Tsutomu Imaizumi, Yoshiyasu Aizawa, Seiji Takatsuki, Kunitake Joo, Masahito Sato, Katsuya Ebe, Yukio Hosaka, Michel Haissaguerre, Keiichi Fukuda
    Journal of the American College of Cardiology 62(11) 1015-1019 2013年09月
    Objectives This study sought to characterize patients with idiopathic ventricular fibrillation (IVF) who develop electrical storms. Background Some IVF patients develop ventricular fibrillation (VF) storms, but the characteristics of these patients are poorly known. Methods Ninety-one IVF patients (86% male) were selected after the exclusion of structural heart diseases, primary electrical diseases, and coronary spasm. Electrocardiogram features were compared between the patients with and without electrical storms. A VF storm was defined as VF occurring ≥3 times in 24 h and J waves > 0.1 mV above the isoelectric line in contiguous leads. Results Fourteen (15.4%) patients had VF storms occurring out-of-hospital at night or in the early morning. J waves were more closely associated with VF storms compared to patients without VF storms: 92.9% versus 36.4% (p < 0.0001). VF storms were controlled by intravenous isoproterenol, which attenuated the J-wave amplitude. After the subsidence of VF storms, the J waves decreased to the nondiagnostic level during the entire follow-up period. Implantable cardioverter-defibrillator therapy was administered to all patients during follow-up. Quinidine therapy was limited, but the patients on disopyramide (n = 3), bepridil (n = 1), or isoprenaline (n = 1) were free from VF recurrence, while VF recurred in 5 of the 9 patients who were not given antiarrhythmic drugs. Conclusions The VF storms in the IVF patients were highly associated with J waves that showed augmentation prior to the VF onset. Isoproterenol was effective in controlling VF and attenuated the J waves, which diminished to below the diagnostic level during follow-up. VF recurred in patients followed up without antiarrhythmic agents. © 2013 by the American College of Cardiology Foundation Published by Elsevier Inc.
  • Common variants at SCN5A-SCN10A and HEY2 are associated with Brugada syndrome, a rare disease with high risk of sudden cardiac death
    Connie R. Bezzina, Julien Barc, Julien Barc, Yuka Mizusawa, Carol Ann Remme, Jean Baptiste Gourraud, Jean Baptiste Gourraud, Jean Baptiste Gourraud, Jean Baptiste Gourraud, Floriane Simonet, Floriane Simonet, Floriane Simonet, Arie O. Verkerk, Peter J. Schwartz, Peter J. Schwartz, Peter J. Schwartz, Peter J. Schwartz, Peter J. Schwartz, Peter J. Schwartz, Lia Crotti, Lia Crotti, Lia Crotti, Federica Dagradi, Federica Dagradi, Pascale Guicheney, Pascale Guicheney, Véronique Fressart, Véronique Fressart, Véronique Fressart, Antoine Leenhardt, Antoine Leenhardt, Antoine Leenhardt, Charles Antzelevitch, Susan Bartkowiak, Eric Schulze-Bahr, Sven Zumhagen, Elijah R. Behr, Rachel Bastiaenen, Jacob Tfelt-Hansen, Jacob Tfelt-Hansen, Morten Salling Olesen, Morten Salling Olesen, Stefan Kääb, Stefan Kääb, Britt M. Beckmann, Peter Weeke, Hiroshi Watanabe, Naoto Endo, Tohru Minamino, Minoru Horie, Seiko Ohno, Kanae Hasegawa, Naomasa Makita, Akihiko Nogami, Wataru Shimizu, Wataru Shimizu, Takeshi Aiba, Philippe Froguel, Philippe Froguel, Philippe Froguel, Beverley Balkau, Beverley Balkau, Olivier Lantieri, Margherita Torchio, Margherita Torchio, Cornelia Wiese, David Weber, Rianne Wolswinkel, Ruben Coronel, Bas J. Boukens, Bas J. Boukens, Stéphane Bézieau, Eric Charpentier, Eric Charpentier, Eric Charpentier, Stéphanie Chatel, Stéphanie Chatel, Stéphanie Chatel, Aurore Despres, Aurore Despres, Aurore Despres, Françoise Gros, Françoise Gros, Françoise Gros, Florence Kyndt, Florence Kyndt, Florence Kyndt, Florence Kyndt, Florence Kyndt, Simon Lecointe, Simon Lecointe, Simon Lecointe, Simon Lecointe, Pierre Lindenbaum, Pierre Lindenbaum, Pierre Lindenbaum, Pierre Lindenbaum, Vincent Portero, Vincent Portero, Vincent Portero
    Nature Genetics 45(9) 1044-1049 2013年09月
    Brugada syndrome is a rare cardiac arrhythmia disorder, causally related to SCN5A mutations in around 20% of cases. Through a genome-wide association study of 312 individuals with Brugada syndrome and 1,115 controls, we detected 2 significant association signals at the SCN10A locus (rs10428132) and near the HEY2 gene (rs9388451). Independent replication confirmed both signals (meta-analyses: rs10428132, P = 1.0 × 10 -68; rs9388451, P = 5.1 × 10 -17) and identified one additional signal in SCN5A (at 3p21; rs11708996, P = 1.0 × 10 -14). The cumulative effect of the three loci on disease susceptibility was unexpectedly large (P trend = 6.1 × 10 -81). The association signals at SCN5A-SCN10A demonstrate that genetic polymorphisms modulating cardiac conduction can also influence susceptibility to cardiac arrhythmia. The implication of association with HEY2, supported by new evidence that Hey2 regulates cardiac electrical activity, shows that Brugada syndrome may originate from altered transcriptional programming during cardiac development. Altogether, our findings indicate that common genetic variation can have a strong impact on the predisposition to rare diseases. © 2013 Nature America, Inc. All rights reserved.
  • A novel SCN5A mutation demonstrating a variety of clinical phenotypes in familial sick sinus syndrome
    Seiko Nakajima, Takeru Makiyama, Koji Hanazawa, Kazuaki Kaitani, Masashi Amano, Yukiko Hayama, Naoaki Onishi, Yodo Tamaki, Makoto Miyake, Toshihiro Tamura, Hirokazu Kondo, Makoto Motooka, Chisato Izumi, Yoshihisa Nakagawa, Minoru Horie
    Internal Medicine 52(16) 1805-1808 2013年08月
    Mutations in SCN5A have been reported to cause several types of hereditary arrhythmias (overlap syndrome). We herein report two patients with the overlapping phenotypes of juvenile sick sinus syndrome (SSS) and Brugada syndrome (BrS). The proband was a man who was in his twenties and had been diagnosed with both SSS and ventricular tachycardia (VT). A pilsicainide challenge test revealed a coved type ST segment elevation. His teenage brother also suffered from SSS, but no VT had been documented. A pilsicainide challenge failed to produce a Brugada-type ST elevation, but there was a marked prolo ngation of the His-ventricle interval. Their electrocardiograms at rest did not display any Brugada-type ST elevations. We identified a novel SCN5A (F1775Lfs*15) mutation in both patients, even though there was a phenotype discrepancy. © 2013 The Japanese Society of Internal Medicine.
  • Identification of a KCNQ1 polymorphism acting as a protective modifier against arrhythmic risk in long-QT syndrome
    Sabine Duchatelet, Lia Crotti, Lia Crotti, Lia Crotti, Rachel A. Peat, Rachel A. Peat, Isabelle Denjoy, Isabelle Denjoy, Hideki Itoh, Myriam Berthet, Myriam Berthet, Seiko Ohno, Véronique Fressart, Maria Cristina Monti, Cristina Crocamo, Matteo Pedrazzini, Federica Dagradi, Federica Dagradi, Alessandro Vicentini, Didier Klug, Paul A. Brink, Althea Goosen, Heikki Swan, Lauri Toivonen, Annukka M. Lahtinen, Kimmo Kontula, Kimmo Kontula, Wataru Shimizu, Minoru Horie, Alfred L. George, David Alexandre Trégouët, David Alexandre Trégouët, Pascale Guicheney, Pascale Guicheney, Peter J. Schwartz, Peter J. Schwartz, Peter J. Schwartz, Peter J. Schwartz
    Circulation: Cardiovascular Genetics 6(4) 354-361 2013年08月
    Background-Long-QT syndrome (LQTS) is characterized by such striking clinical heterogeneity that, even among family members carrying the same mutation, clinical outcome can range between sudden death and no symptoms. We investigated the role of genetic variants as modifiers of risk for cardiac events in patients with LQTS. Methods and Results-In a matched case-control study including 112 patient duos with LQTS from France, Italy, and Japan, 25 polymorphisms were genotyped based on either their association with QTc duration in healthy populations or on their role in adrenergic responses. The duos were composed of 2 relatives harboring the same heterozygous KCNQ1 or KCNH2 mutation: 1 with cardiac events and 1 asymptomatic and untreated. The findings were then validated in 2 independent founder populations totaling 174 symptomatic and 162 asymptomatic patients with LQTS, and a metaanalysis was performed. The KCNQ1 rs2074238 T-allele was significantly associated with a decreased risk of symptoms 0.34 (0.19-0.61; P < 0.0002) and with shorter QTc (P < 0.0001) in the combined discovery and replication cohorts. Conclusions-We provide evidence that the KCNQ1 rs2074238 polymorphism is an independent risk modifier with the minor T-allele conferring protection against cardiac events in patients with LQTS. This finding is a step toward a novel approach for risk stratification in patients with LQTS. © 2013 American Heart Association, Inc.
  • Spontaneous coronary artery spasm accidentally detected by 320-row multi-detector computed tomography
    Tamiro Kawaguchi, Hideki Hayashi, Nobu Naiki, Hiroshi Sakai, Takashi Yamamoto, Masatoshi Fujita, Minoru Horie
    Journal of Cardiology Cases 8(2) 85-87 2013年08月
    A 64-year-old woman was introduced to our hospital suspected of having angina pectoris. A 12-lead electrocardiogram showed negative T wave in inferior leads. An echocardiography revealed no abnormality. In 320-row multi-detector computed tomography (MDCT), a severe narrowing of the right coronary artery was detected with collateral vessels between the distal portion of the obstructed right coronary artery and the left anterior descending artery. Coronary angiography showed no stenosis of the right coronary artery and non-obstructive plaques in the left coronary artery. To provoke coronary artery spasm, acetylcholine was infused into the left coronary artery. But, no narrowing was inducible in the left coronary artery. After that, a spasm of the right coronary artery was observed without the injection of acetylcholine into the right coronary artery. The spasm was located in the same site as the narrowing on MDCT imaging. A calcium channel antagonist (benidipine hydrochloride 8. mg/day) and a nitrate (isosorbide dinitrate 80. mg) were effective for coronary artery spasm. < . Learning objective: Multi-detector computed tomography (MDCT) imaging is useful for examining coronary artery disease. In addition to evaluating coronary organic stenosis, 320-row MDCT could detect spontaneous coronary artery spasm. Although coronary artery spasm has to be taken into account, intracoronary injection of acetylcholine is necessary to diagnose coronary artery spasm. > . © 2013 Japanese College of Cardiology.
  • Pitfall of the meta-analysis regarding early repolarization pattern
    Hideki Hayashi, Yoshitaka Murakami, Minoru Horie
    Journal of the American College of Cardiology 62(1) 86 2013年07月
  • 家族性心房細動 (特集 最新の心房細動の診療) -- (各種病態における心房細動の治療と管理)
    堀江 稔
    臨牀と研究 90(9) 1210-1214 2013年09月
  • Genetic background of catecholaminergic polymorphic ventricular tachycardia in Japan
    Mihoko Kawamura, Seiko Ohno, Nobu Naiki, Iori Nagaoka, Kenichi Dochi, Qi Wang, Kanae Hasegawa, Hiromi Kimura, Akashi Miyamoto, Yuka Mizusawa, Hideki Itoh, Takeru Makiyama, Naokata Sumitomo, Hiroya Ushinohama, Kotaro Oyama, Nobuyuki Murakoshi, Kazutaka Aonuma, Hitoshi Horigome, Takafumi Honda, Masao Yoshinaga, Makoto Ito, Minoru Horie
    Circulation Journal 77(7) 1705-1713 2013年07月
    Background: The genetic background of catecholaminergic polymorphic ventricular tachycardia (CPVT) has been extensively investigated for the last decade in Western countries, but it remains unstudied in the Asian population. Methods and Results: In 50 Japanese probands from unrelated families who satisfied clinical criteria for CPVT, genetic testing was conducted in all exons on 3 CPVT-related genes: cardiac ryanodine receptor 2 (RYR2), calsequestrin 2 (CASQ2) and inward rectifier potassium channel 2 (KCNJ2), and the clinical features between RYR2-genotyped and -non-genotyped patient groups were compared. Genetic and clinical evaluation was also done in 46 family members. In the genetic screening, 28 (18 novel) RYR2 (56.0%), 1 compound heterozygous CASQ2 (2.0%) and 1 KCNJ2 (2.0%) mutation carriers were identified. In the RYR2 mutation-positive group, the frequency of bidirectional ventricular tachycardia and the use of β-blockers were significantly higher than in the mutation-negative group. In contrast, there was no significant difference in supraventricular arrhythmias between the 2 groups. With regard to disease penetrance, the number of family members of RYR2-genotyped probands with a clinical diagnosis of CPVT was high. Conclusions: Thirty gene mutation carriers were found for 3 genes in 50 probands clinically diagnosed as having CPVT. The penetrance of CPVT phenotype was significantly higher in RYR2 mutation carriers, thus RYR2 gene screening in CPVT patients would be indispensable to prevent unexpected cardiac sudden death of young family members.
  • 座談会 致死性不整脈診療の現状と今後の展望 (特集 致死性不整脈診療の最前線)
    堀江 稔, 田中 敏博, 渡部 裕
    最新医学 68(7) 1509-1519 2013年07月
  • 嚢胞性線維症 (第1土曜特集 イオンチャネル病のすべて)
    堀江 稔
    医学のあゆみ 245(9) 727-731 2013年06月
  • 不整脈源性右室心筋症
    堀江 稔
    循環器内科 73(4) 437-442 2013年04月
  • QT延長症候群 (特集 救急医療に必要な不整脈診療の実際) -- (知っておくと役立つ不整脈の知識)
    堀江 稔
    救急医学 = The Japanese journal of acute medicine 37(2) 218-223 2013年02月
  • 磯貝論文に対するEditorial Comment
    堀江 稔
    心臓 45(9) 1129-1129 2013年
  • 器質的心疾患を認めない不整脈の学校生活管理指導ガイドライン(2013年改訂版)
    吉永 正夫, 泉田 直己, 岩本 眞理, 牛ノ濱 大也, 住友 直方, 田内 宣生, 高橋 良明, 富田 英, 長嶋 正實, 堀米 仁志, 山内 邦昭, 阿部 勝已, 新垣 義夫, 上野 倫彦, 太田 邦雄, 佐藤 誠一, 高木 純一, 立野 滋, 檜垣 高史, 市田 蕗子, 白石 裕比湖, 杉 薫, 堀江 稔
    日本小児循環器学会雑誌 29(6) 277-290 2013年
  • スプライシング異常と循環器疾患
    脇坂 啓子, 堀江 稔
    循環器内科 70(5) 523-529 2011年11月
  • 3.日本におけるブルガダ症候群:診断と治療
    堀江 稔
    日本内科学会雑誌 100(0) 91b-92a 2011年
  • 致死性不整脈と遺伝子異常
    堀江 稔
    心臓 43(10) 1291-1296 2011年
  • 低酸素脳症が残存したカテコラミン誘発性心室頻拍の1例
    脇屋 桃子, 久次米 真吾, 伊藤 尚志, 榎本 善成, 森山 明義, 沼田 綾香, 熊谷 賢太, 酒井 毅, 坂田 隆夫, 野呂 眞人, 杉 薫, 堀江 稔
    心臓 43(2) S2_81-S2_85 2011年
    症例: 14歳, 男性.
    経過: 12歳ごろより運動後に前失神症状を自覚していた. 運動後に心肺停止となり緊急搬送となった. 来院時は心室細動で, 循環動態は破綻していた. 直流通電施行後も, 持続性心室頻拍が頻回に出現した. 人工呼吸器管理下で体外補助循環, 低体温療法を施行したが, 低酸素脳症が残存した. 洞調律復帰後の心電図に経時的な異常は認めなかった. 心臓電気生理学的検査では, 無投薬下では病的不整脈は誘発されず, イソプロテレノール, ノルエピネフリンおよびエピネフリンを負荷した時点で, 単相性心室期外収縮が自然に出現するのみであった. 低酸素脳症のために運動負荷誘発試験は試行できなかった. QT延長症候群やBrugada症候群は否定的であった. 臨床経過よりカテコラミン誘発性心室頻拍が疑われ, 家族の強い希望で植込み型除細動器の植え込みを施行した.
    結語: カテコラミン誘発性心室頻拍と臨床的診断した1例であった. 若年の運動後, 意識消失の既往がある症例を診察する際には, 本症例を鑑別診断にあげる必要がある.
  • ペースメーカ植込み同胞例に認められた新たなLamin A/C変異
    佐野 幹, 渡邉 英一, 牧山 武, 内山 達司, 祖父江 嘉洋, 奥田 健太郎, 山本 真由美, 堀江 稔, 尾崎 行男
    心電図 31(1) 18-24 2011年
    中間径線維のひとつであるLamin A/Cは,核膜内膜を裏打ちして核膜構造を維持するとともに,遺伝子転写調節や遺伝子発現制御などの機能を有する.Lamin A/C遺伝子(LMNA)は,関節拘縮,骨格筋異常,および刺激伝導障害に伴う拡張型心筋症を3主徴とするEmery-Dreifuss型筋ジストロフィーの責任遺伝子として報告された.その後,関節拘縮や骨格筋異常を有さないものの,拡張型心筋症に刺激伝導障害を合併した症例にLMNA変異を認めることが報告され,Lamin関連心筋症とよばれる.本疾患は心不全に加え,心室性頻脈性不整脈による突然死が多いのを特徴とする.今回,われわれは,徐脈性不整脈の治療目的にペースメーカを植込まれた3同胞(ペースメーカ植込み時平均年齢49.6歳,男性:女性=1例:2例)に遺伝子検索を行い,新たなLMNA変異(Q258X)を認めたため,文献的な考察を加えて報告する.
  • フォーラム 第74回日本循環器学会総会・学術集会レポート(Vol.4)シンポジウム4 遺伝性不整脈の診断と治療(Inherited Arrhythmias: Diagnosis and Treatment)
    堀江 稔
    医学のあゆみ 233(7) 559-561 2010年05月
  • 心エコー検査における左室拡張機能の指標と血漿BNP値の比較検討
    石垣 多佳子, 蔦本 尚慶, 泉 裕美, 藤澤 義久, 清水 祥子, 五十川 静男, 吉田 孝, 岡部 英俊, 堀江 稔
    超音波検査技術 35(4) 411-417 2010年
  • Emerging acute unilateral pulmonary edema in a patient with pheochromocytoma.
    Itsuko Miyazawa, Atsuyuki Wada, Toshiro Sugimoto, Norihisa Nitta, Minoru Horie
    Int J Cardiol 133(2) 50-51 2009年04月
    We report a patient who presented with unilateral pulmonary edema without cardiomegaly. Our patient was finally diagnosed as having pheochromocytoma crisis. © 2007 Elsevier Ireland Ltd. All rights reserved.
  • デスモゾーム病としての不整脈源性右室心筋症--デスモゾーム分子遺伝子異常 (第5土曜特集 心不全--研究と臨床の最前線) -- (心不全の先端的研究トピックス 心不全のジェネティクスとエピジェネティクス)
    堀江 稔
    医学のあゆみ 232(5) 588-592 2010年01月
  • Interaction between dietary marine-derived n-3 fatty acids intake and J-point elevation on the risk of cardiac death: A 24-year follow-up of Japanese men
    Takashi Hisamatsu, Takashi Hisamatsu, Takashi Hisamatsu, Katsuyuki Miura, Katsuyuki Miura, Takayoshi Ohkubo, Takayoshi Ohkubo, Takashi Yamamoto, Akira Fujiyoshi, Naoko Miyagawa, Aya Kadota, Naoyuki Takashima, Nagako Okuda, Yasuhiro Matsumura, Katsushi Yoshita, Yoshikuni Kita, Yoshitaka Murakami, Yoshitaka Murakami, Yasuyuki Nakamura, Tomonori Okamura, Minoru Horie, Akira Okayama, Hirotsugu Ueshima, Hirotsugu Ueshima
    Heart 99(14) 1024-1029 2013年07月
    Objective: Higher marine-derived n-3 fatty acids (MDn3FAs) intake reduces the risk of sudden cardiac death via antiarrhythmic effects. The article evaluates whether MDn3FAs intake attenuates the increased risk of cardiac death associated with J-point elevation (JPE), characterised by an elevation of QRS-ST junction (J-point) ≥0.1 mV on electrocardiography. Design: A prospective population-based cohort study. Setting: The National Survey on Circulatory Disorders and the National Nutrition Survey of Japan. Participants: A total of 4348 community-dwelling men (mean age 49.3 years), without cardiovascular diseases at baseline, from randomly selected areas across Japan. Main outcome measures: Cardiac death (200 men) during the 24-year follow-up. Results: Dietary MDn3FAs intake was assessed using a dietary method to estimate individual intake of household-based weighed food records for 3 days. Cox models were used to calculate HRs and 95% CIs adjusted for possible confounding factors. JPE was present in 340 participants (7.8%). The median daily intake of MDn3FAs was 0.35%kcal (0.92 g/day). The risk of cardiac death was significantly higher in participants with JPE than in those without JPE in the low intake group ( < 0.35%kcal; adjusted HR 3.51; 95% CI 1.84 to 6.73; p < 0.001), but not in the high intake group (≥0.35%kcal; adjusted HR 1.09; 95% CI 0.56 to 2.16; p=0.795). The interaction between dietary MDn3FAs intake and JPE on the risk of cardiac death was statistically significant (p=0.006). Conclusions: The increased risk of cardiac death associated with JPE may be attenuated by higher dietary MDn3FAs intake.
  • 不整脈の遺伝子診断  2.家族性ペースメーカー植込み症例における遺伝的背景の検討―心臓Na`+´チャネル病,Lamin A/C遺伝子関連心筋症―:―心臓Na+チャネル病,Lamin A/C遺伝子関連心筋症―
    牧山 武, 静田 聡, 赤尾 昌治, 木村 剛, 堀江 稔
    心電図 30(3) 200-208 2010年
    洞不全症候群,房室ブロックに代表される徐脈性不整脈疾患は,加齢性変化にて多くみられるが,若年や家族性に認められる場合には遺伝的素因の関与が強く疑われる.今回われわれは,家族性徐脈性不整脈疾患の遺伝的背景を調べるために,家族性ペースメーカー植込み患者33症例(すべて発端者)を対象として候補遺伝子の網羅的スクリーニングを施行した.遺伝子解析の結果,33例中17例(51.5%)に心臓Na+チャネル遺伝子(SCN5A),またはLamin A/C遺伝子(LMNA)異常を同定した〔SCN5A異常8/33例(24.2%),LMNA異常9/33例(27.2%)〕.SCN5A異常を検出した8例中5例には,ほかの心臓Na+チャネル病の合併(Brugada症候群4例,QT延長症候群1例)を認めた.一方,LMNAは核膜の裏打ち蛋白であるLamin A,Cをコードし,その遺伝子異常により拡張型心筋症,心臓伝導障害,致死性心室性不整脈による突然死を引き起こす.本研究の結果,家族性ペースメーカー植込み患者には,突然死を引き起こし得る心臓Na+チャネル病(Brugada症候群,QT延長症候群)やLamin A/C遺伝子関連心筋症を合併している例が少なくないことがわかった.治療としては,ペースメーカー植込みではなく,植込み型除細動器や除細動機能付き両室ペーシング植込みが望ましい例もあり,家族性徐脈性不整脈症例における遺伝子解析の重要性が示唆された.
  • L-Type calcium channel mutations in Japanese patients with inherited arrhythmias
    Megumi Fukuyama, Seiko Ohno, Seiko Ohno, Qi Wang, Hiromi Kimura, Takeru Makiyama, Hideki Itoh, Makoto Ito, Minoru Horie
    Circulation Journal 77(7) 1799-1806 2013年07月
    Background: Mutations in genes encoding the L-type cardiac calcium channel (LTCC) are associated with various types of inherited arrhythmias, including Brugada syndrome (BrS). However, the frequency in Asian populations remains unknown. This study aimed to elucidate disease-causing mutations in LTCC-related genes in Japanese patients diagnosed as BrS or idiopathic ventricular fibrillation (IVF), early repolarization syndrome, short QT syndrome, and compare them with those carrying SCN5A mutations. Methods and Results: We screened CACNA1C and CACNB2b in 312 probands and compared the clinical characteristics between probands with gene mutations in CACNA1C or SCN5A. In results, we identified 6 CACNA1C mutations in 7 unrelated probands and SCN5A mutations in 20 probands. There were no CACNB2b mutation carriers. In topology, half of the mutations were located in the C-terminus. Among 7 CACNA1C mutation carriers, 2 were female and 3 were symptomatic; 2 patients were resuscitated from ventricular fibrillation, and 1 patient had syncope. Compared with SCN5A mutation carriers, there were no significant differences in the ECG characteristics. 2 of 3 symptomatic CACNA1C patients were female, but all female SCN5A mutation carriers remained asymptomatic. Conclusions: We identified 6 CACNA1C mutations in BrS and IVF patients and their phenotypes were varied. Although mutation frequency was not high, screening of LTCC channel genes may be clinically important to prevent unexpected sudden death. (Circ J 2013; 77: 1799-1806).
  • 心不全マーカーと心血管リスク予測因子としてのナトリウム利尿ペプチド
    蔦本 尚慶, 堀江 稔
    臨床薬理 40(4) 173S-174S 2009年
  • 心血管疾患 (特集 全身疾患としてのCOPD)
    松本 鉄也, 中野 恭幸, 堀江 稔
    日本胸部臨床 67(12) 1000-1009 2008年12月
  • 家族性心臓伝導障害に同定されたconnexin 40遺伝子GJA5変異の機能異常
    蒔田 直昌, 住友 直方, 関 明子, 渡部 裕, 福原 茂朋, 牧山 武, 堀江 稔, 萩原 誠久, 望月 直樹, Jean-Jacques Schott
    心電図 30(3) 2010年
  • Restoration of aberrant conduction induced by premature ventricular contractions
    Hideki Hayashi, Takeshi Shibukawa, Minoru Horie
    Internal Medicine 52(12) 1425-1425 2013年06月
  • 不整脈の遺伝子診断  1.先天性QT延長症候群の遺伝子診断―複数変異症例の検討―:―複数変異症例の検討―
    伊藤 英樹, 清水 渉, 林 研至, 山形 研一郎, 坂口 知子, 大野 聖子, 牧山 武, 赤尾 昌治, 藍 智彦, 野田 崇, 宮崎 文, 宮本 恵宏, 山岸 正和, 鎌倉 史郎, 堀江 稔
    心電図 30(3) 195-199 2010年
    先天性QT延長症候群は,イオンチャネル蛋白に関連する遺伝子変異が原因で心筋再分極異常をきたし,QT延長と致死性不整脈を発症させる疾患である.通常遺伝子変異は単変異であるが,複数の変異を有する症例も報告されている.全国4施設で遺伝子変異が同定された612症例の先天性QT延長症候群を単変異574例(LQT1 259例,LQT2 251例,LQT3 62例,LQT5 2例)と複数変異38例に分類し,臨床像を比較検討した.遺伝子診断された314例の発端者のうち,28例(8.9%)が複数変異症例であった.全612例の解析において,QTc間隔は複数変異症例で有意に延長しており(複数変異症例vs.単変異症例;501±58 vs. 477±53 msec, p=0.014),発症年齢も若年であった(複数変異症例vs.単変異症例;10±7 vs. 18±16歳,p<0.001).β遮断薬の内服率は複数変異症例で有意に高率であった.40歳未満の心イベントはどのサブタイプの単変異症例より,複数変異症例で高率であった.以上から,複数変異症例を有するQT延長症候群例の臨床像は単変異症例より重篤であることが示唆された.
  • Is More Aggressive Prevention of Coronary Artery Disease Required for Patients With Early Repolarization Syndrome?: Reply
    Takashi Hisamatsu, Takashi Hisamatsu, Takayoshi Ohkubo, Katsuyuki Miura, Minoru Horie, Hirotsugu Ueshima, Hirotsugu Ueshima
    Circulation Journal 77(6) 1643 2013年05月
  • Age-dependent clinical and genetic characteristics in Japanese patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia
    Seiko Ohno, Seiko Ohno, Iori Nagaoka, Megumi Fukuyama, Hiromi Kimura, Hideki Itoh, Takeru Makiyama, Akihiko Shimizu, Minoru Horie
    Circulation Journal 77(6) 1534-1542 2013年05月
    Background: Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a heart muscle disease caused by desmosomal gene mutations, and presents as ventricular tachycardia and sudden cardiac death. Although the mean age at onset or diagnosis of ARVC/D are reported to be around the 30-40 s, the age-dependent clinical and genetic differences remain unknown. Methods and Results: A total of 35 consecutive Japanese probands (23 male) who were clinically diagnosed with ARVC/D were enrolled in the present study, and genetic analysis of PKP2, DSP, DSG2, and DSC2 was done. The mean age at the first symptom and at diagnosis was 38.6±14.8 years and 40.5±17.7 years, respectively. Probands in whom the onset was cardiopulmonary arrest were significantly younger (22.3±15.3 years) than those with arrhythmia (41.1±13.2 years) or congestive heart failure (45.7±8.5 years). On genetic screening, 19 mutation carriers were identified. Although there was no age dependence for each gene mutation carrier, carriers with PKP2 premature stop codon developed the disease at a significantly younger age than other mutation carriers. Conclusions: The initial clinical manifestations in some young probands were very severe, and PKP2 mutations with a premature stop codon would be associated with disease onset at a younger age.
  • SCN5A mutation associated with ventricular fibrillation, early repolarization, and concealed myocardial abnormalities
    Hiroshi Watanabe, Kimie Ohkubo, Ichiro Watanabe, Taka Aki Matsuyama, Hatsue Ishibashi-Ueda, Nobue Yagihara, Wataru Shimizu, Minoru Horie, Tohru Minamino, Naomasa Makita
    International Journal of Cardiology 165(2) 21-23 2013年05月
  • Association between J-point elevation and death from coronary artery disease: 15-year follow-up of the NIPPON DATA90
    Takashi Hisamatsu, Takashi Hisamatsu, Takayoshi Ohkubo, Takayoshi Ohkubo, Katsuyuki Miura, Takashi Yamamoto, Akira Fujiyoshi, Naoko Miyagawa, Aya Kadota, Naoyuki Takashima, Shin ya Nagasawa, Yoshikuni Kita, Yoshitaka Murakami, Akira Okayama, Minoru Horie, Tomonori Okamura, Hirotsugu Ueshima, Hirotsugu Ueshima
    Circulation Journal 77(5) 1260-1266 2013年05月
    Background: An early repolarization pattern, characterized by an elevation of the QRS-ST junction (J-point) on 12-lead electrocardiography (ECG) is associated with cardiac and sudden death. However, little is known about the prognostic significance of J-point elevation for various disease-specific cardiovascular outcomes, including coronary artery disease (CAD). Methods and Results: To investigate the association between the presence of J-point elevation ≥0.1 mV and various disease-specific cardiovascular outcomes, we conducted a 15-year prospective study in a representative general Japanese population of 7,630 individuals (41% men, mean age 52.4 years) who participated in the National Survey of Circulatory Disorders. Cox models were used to estimate the hazard ratios (HRs) adjusted for possible confounding factors. J-point elevation was present in 264 individuals (3.5%) and was associated with an increased risk of cardiac death (adjusted HR, 2.54; 95% confidence interval [CI] 1.40-4.58; P=0.002) and death from CAD (adjusted HR, 4.66; 95% CI 2.30-9.46; P < 0.001). In a subgroup analysis by age, the association between J-point elevation and cardiovascular outcomes was more remarkable in middle-aged ( < 60 years) than in older individuals (≥60 years) (all P for interaction < 0.05). Conclusions: J-point elevation on standard 12-lead ECG was an independent predictor of cardiac death and death from CAD in a representative sample of the general Japanese population, particularly among the middle-aged.
  • CARTO (Up-to-Date Art&Technique 進化した3Dイメージング(前編)CT・MRIの見かた・撮りかた)
    小澤 友哉, 堀江 稔
    Circulation up-to-date 8(3) 270-279 2013年06月
  • Ultrastructural maturation of human-induced pluripotent stem cell-derived cardiomyocytes in a long-term culture
    Tsukasa Kamakura, Takeru Makiyama, Kenichi Sasaki, Yoshinori Yoshida, Yimin Wuriyanghai, Jiarong Chen, Tetsuhisa Hattori, Seiko Ohno, Toru Kita, Minoru Horie, Shinya Yamanaka, Takeshi Kimura
    Circulation Journal 77(5) 1307-1314 2013年05月
    Background: In the short- to mid-term, cardiomyocytes generated from human-induced pluripotent stem cells (hiPSC-CMs) have been reported to be less mature than those of adult hearts. However, the maturation process in a long-term culture remains unknown. Methods and Results: A hiPSC clone generated from a healthy control was differentiated into CMs through embryoid body (EB) formation. The ultrastructural characteristics and gene expressions of spontaneously contracting EBs were analyzed through 1-year of culture after cardiac differentiation was initiated. The 14-day-old EBs contained a low number of myofibrils, which lacked alignment, and immature high-density Z-bands lacking A-, H-, I-, and Mbands. Through the long-term culture up to 180 days, the myofibrils became more tightly packed and formed parallel arrays accompanied by the appearance of mature Z-, A-, H-, and I-bands, but not M-bands. Notably, M-bands were finally detected in 360-day-old EBs. The expression levels of the M-band-specific genes in hiPSC-CMs remained lower in comparison with those in the adult heart. Immunocytochemistry indicated increasing number of MLC2v-positive/MLC2a-negative cells with decreasing number of MLC2v/MLC2a double-positive cells, indicating maturing of ventricular-type CMs. Conclusions: The structural maturation process of hiPSC-CMs through 1-year of culture revealed ultrastructural sarcomeric changes accompanied by delayed formation of M-bands. Our study provides new insight into the maturation process of hiPSC-CMs.
  • Novel SCN3B mutation associated with brugada syndrome affects intracellular trafficking and function of Nav1.5
    Taisuke Ishikawa, Naohiko Takahashi, Seiko Ohno, Harumizu Sakurada, Kazufumi Nakamura, Young Keun On, Jeong Euy Park, Takeru Makiyama, Minoru Horie, Takuro Arimura, Naomasa Makita, Akinori Kimura
    Circulation Journal 77(4) 959-967 2013年04月
    Background: Brugada syndrome (BrS) is characterized by specific alterations on ECG in the right precordial leads and associated with ventricular arrhythmia that may manifest as syncope or sudden cardiac death. The major causes of BrS are mutations in SCN5A for a large subunit of the sodium channel, Nav1.5, but a mutation in SCN3B for a small subunit of sodium channel, Navβ3, has been recently reported in an American patient. Methods and Results: A total of 181 unrelated BrS patients, 178 Japanese and 3 Koreans, who had no mutations in SCN5A, were examined for mutations in SCN3B by direct sequencing of all exons and adjacent introns. A mutation, Val110Ile, was identified in 3 of 178 (1.7%) Japanese patients, but was not found in 480 Japanese controls. The SCN3B mutation impaired the cytoplasmic trafficking of Nav1.5, the cell surface expression of which was decreased in transfected cells. Whole-cell patch clamp recordings of the transfected cells revealed that the sodium currents were significantly reduced by the SCN3B mutation. Conclusions: The Val110Ile mutation of SCN3B is a relatively common cause of SCN5A-negative BrS in Japan, which has a reduced sodium current because of the loss of cell surface expression of Nav1.5.
  • A Nonsynonymous Polymorphism in Semaphorin 3A as a Risk Factor for Human Unexplained Cardiac Arrest with Documented Ventricular Fibrillation
    Yukiko Nakano, Yukiko Nakano, Kazuaki Chayama, Kazuaki Chayama, Hidenori Ochi, Hidenori Ochi, Masaaki Toshishige, Yasufumi Hayashida, Daiki Miki, Daiki Miki, C. Nelson Hayes, C. Nelson Hayes, Hidekazu Suzuki, Takehito Tokuyama, Noboru Oda, Kazuyoshi Suenari, Yuko Uchimura-Makita, Kenta Kajihara, Akinori Sairaku, Chikaaki Motoda, Mai Fujiwara, Yoshikazu Watanabe, Yukihiko Yoshida, Kimie Ohkubo, Ichiro Watanabe, Akihiko Nogami, Kanae Hasegawa, Hiroshi Watanabe, Naoto Endo, Takeshi Aiba, Wataru Shimizu, Seiko Ohno, Minoru Horie, Koji Arihiro, Satoshi Tashiro, Naomasa Makita, Yasuki Kihara
    PLoS Genetics 9(4) 2013年04月
    Unexplained cardiac arrest (UCA) with documented ventricular fibrillation (VF) is a major cause of sudden cardiac death. Abnormal sympathetic innervations have been shown to be a trigger of ventricular fibrillation. Further, adequate expression of SEMA3A was reported to be critical for normal patterning of cardiac sympathetic innervation. We investigated the relevance of the semaphorin 3A (SEMA3A) gene located at chromosome 5 in the etiology of UCA. Eighty-three Japanese patients diagnosed with UCA and 2,958 healthy controls from two different geographic regions in Japan were enrolled. A nonsynonymous polymorphism (I334V, rs138694505A > G) in exon 10 of the SEMA3A gene identified through resequencing was significantly associated with UCA (combined P = 0.0004, OR 3.08, 95%CI 1.67-5.7). Overall, 15.7% of UCA patients carried the risk genotype G, whereas only 5.6% did in controls. In patients with SEMA3A I334V , VF predominantly occurred at rest during the night. They showed sinus bradycardia, and their RR intervals on the 12-lead electrocardiography tended to be longer than those in patients without SEMA3A I334V (1031±111 ms versus 932±182 ms, P = 0.039). Immunofluorescence staining of cardiac biopsy specimens revealed that sympathetic nerves, which are absent in the subendocardial layer in normal hearts, extended to the subendocardial layer only in patients with SEMA3A I334V . Functional analyses revealed that the axon-repelling and axon-collapsing activities of mutant SEMA3A I334V genes were significantly weaker than those of wild-type SEMA3A genes. A high incidence of SEMA3A I334V in UCA patients and inappropriate innervation patterning in their hearts implicate involvement of the SEMA3A gene in the pathogenesis of UCA. © 2013 Nakano et al.
  • Effects of flecainide on exercise-induced ventricular arrhythmias and recurrences in genotype-negative patients with catecholaminergic polymorphic ventricular tachycardia
    Hiroshi Watanabe, Christian Van Der Werf, Ferran Roses-Noguer, Arnon Adler, Naokata Sumitomo, Christian Veltmann, Raphael Rosso, Zahurul A. Bhuiyan, Hennie Bikker, Prince J. Kannankeril, Minoru Horie, Tohru Minamino, Sami Viskin, Björn C. Knollmann, Jan Till, Arthur A.M. Wilde
    Heart Rhythm 10(4) 542-547 2013年04月
    Background: Conventional therapy with beta-blockers is incompletely effective in preventing arrhythmic events in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT). We have previously discovered that flecainide in addition to conventional drug therapy prevents ventricular arrhythmias in patients with genotype-positive CPVT. Objective: To study the efficacy of flecainide in patients with genotype-negative CPVT. Methods: We studied the efficacy of flecainide for reducing ventricular arrhythmias during exercise testing and preventing arrhythmia events during long-term follow-up. Results: Twelve patients with genotype-negative CPVT were treated with flecainide. Conventional therapy failed to control ventricular arrhythmias in all patients. Flecainide was initiated because of significant ventricular arrhythmias (n = 8), syncope (n = 3), or cardiac arrest (n = 1). At the baseline exercise test before flecainide, 6 patients had ventricular tachycardia and 5 patients had bigeminal or frequent ventricular premature beats. Flecainide reduced ventricular arrhythmias at the exercise test in 8 patients compared to conventional therapy, similar to that in patients with genotype-positive CPVT in our previous report. Notably, flecainide completely prevented ventricular arrhythmias in 7 patients. Flecainide was continued in all patients except for one who had ventricular tachycardia at the exercise test on flecainide. During a follow-up of 48±94 months, arrhythmia events (sudden cardiac death and aborted cardiac arrest) associated with noncompliance occurred in 2 patients. Flecainide was not discontinued owing to side effects in any of the patients. Conclusions: Flecainide was effective in patients with genotype-negative CPVT, suggesting that spontaneous Ca 2+ release from ryanodine channels plays a role in arrhythmia susceptibility, similar to that in patients with genotype-positive CPVT. © 2013 Published by Elsevier Inc. on behalf of Heart Rhythm Society.
  • Long-term follow-up of a pediatric cohort with short QT syndrome
    Juan Villafañe, Joseph Atallah, Michael H. Gollob, Philippe Maury, Christian Wolpert, Roman Gebauer, Hiroshi Watanabe, Minoru Horie, Olli Anttonen, Prince Kannankeril, Brett Faulknier, Jorge Bleiz, Takeru Makiyama, Wataru Shimizu, Robert M. Hamilton, Ming Lon Young
    Journal of the American College of Cardiology 61(11) 1183-1191 2013年03月
    Objectives: The purpose of this study was to define the clinical characteristics and long-term follow-up of pediatric patients with short QT syndrome (SQTS). Background: SQTS is associated with sudden cardiac death. The clinical characteristics and long-term prognosis in young patients have not been reported. Methods: This was an international case series involving 15 centers. Patients were analyzed for electrocardiography characteristics, genotype, clinical events, Gollob score, and efficacy of medical or defibrillator (implantable cardioverter-defibrillator [ICD]) therapy. To assess the possible prognostic value of the Gollob score, we devised a modified Gollob score that excluded clinical events from the original score. Results: Twenty-five patients 21 years of age or younger (84% males, median age: 15 years, interquartile range: 9 to 18 years) were followed up for 5.9 years (interquartile range: 4 to 7.1 years). Median corrected QT interval for heart rate was 312 ms (range: 194 to 355 ms). Symptoms occurred in 14 (56%) of 25 patients and included aborted sudden cardiac death in 6 patients (24%) and syncope in 4 patients (16%). Arrhythmias were common and included atrial fibrillation (n = 4), ventricular fibrillation (n = 6), supraventricular tachycardia (n = 1), and polymorphic ventricular tachycardia (n =1). Si xteen patients (84%) had a familial or personal history of cardiac arrest. A gene mutation associated with SQTS was identified in 5 (24%) of 21 probands. Symptomatic patients had a higher median modified Gollob score (excluding points for clinical events) compared with asymptomatic patients (5 vs. 4, p = 0.044). Ten patients received medical treatment, mainly with quinidine. Eleven of 25 index cases underwent ICD implantation. Two patients had appropriate ICD shocks. Inappropriate ICD shocks were observed in 64% of patients. Conclusions: SQTS is associated with aborted sudden cardiac death among the pediatric population. Asymptomatic patients with a Gollob score of < 5 remained event free, except for an isolated episode of supraventricular tachycardia, over an average 6-year follow-up. A higher modified Gollob score of 5 or more was associated with the likelihood of clinical events. Young SQTS patients have a high rate of inappropriate ICD shocks. © 2013 by the American College of Cardiology Foundation.
  • Prognostic implications of progressive cardiac conduction disease
    Tamiro Kawaguchi, Hideki Hayashi, Akashi Miyamoto, Tomohide Yoshino, Atsushi Taniguchi, Nobu Naiki, Yoshihisa Sugimoto, Makoto Ito, Joel Q. Xue, Yoshitaka Murakami, Minoru Horie
    Circulation Journal 77(1) 60-67 2013年01月
    Background: Progressive cardiac conduction disease (PCCD), characterized by temporal increase in PR interval and QRS duration, may be attributed to diverse pathophysiological mechanisms. This study aimed to investigate whether PCCD is associated with increased risk of cardiovascular morbidity and mortality. Methods and Results: Digital analysis of 12-lead ECG was performed to select patients with PCCD from among a database containing 359,737 ECGs. Long-term prognosis of PCCD was assessed in a large hospital-based population: 458 patients (341 males; mean age, 57.9±14.7 years) with PCCD were enrolled. During a mean followup of 13.3±6.4 year s, 109 patients were hospitalized for heart failure (HF), and there were 16 and 59 deaths from cardiovascular diseases and all causes, respectively. Multivariate Cox proportional hazards analysis confirmed (1) a significant association of temporal incremental rate of PR interval (≥2 ms/year) and QRS duration (≥3 ms/year) with HF hospitalization (hazard ratio [HR], 2.34; 95% confidence interval [CI] , 1.36-4.05; P=0.002 and HR, 2.08; 95% CI, 1.25-3.53; P=0.01, respectively) and (2) a significant association of temporal incremental rate of PR interval (≥4 ms/year) and QRS duration (≥5 ms/year) with cardiovascular mortality (HR, 6.9; 95% CI, 1.47-36.96; P=0.02 and HR, 4.31; 95% CI, 1.19-16.5; P=0.03, respectively). Conclusions: The severity of PCCD was independently and significantly associated with HF hospitalization and cardiovascular mortality.
  • Flecainide reduces ventricular arrhythmias via a mechanism that differs from that of β-blockers in catecholaminergic polymorphic ventricular tachycardia
    Kenichi Dochi, Hiroshi Watanabe, Mihoko Kawamura, Akashi Miyamoto, Tomoya Ozawa, Yuko Nakazawa, Takashi Ashihara, Seiko Ohno, Hideki Hayashi, Makoto Ito, Hisanori Sakazaki, Hiro Kawata, Hiroya Ushinohama, Richard H. Kaszynski, Tohru Minamino, Naokata Sumitomo, Wataru Shimizu, Minoru Horie
    Journal of Arrhythmia 29(5) 255-260 2013年01月
    Background: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmia syndrome characterized by episodic ventricular tachycardia induced by adrenergic stress. Although β-blockers are used as first-line therapy, their therapeutic effects are largely incomplete. Flecainide has recently been shown to modify the molecular defects in CPVT. The aim of this study was to investigate the effects of flecainide as an add-on to conventional therapy on exercise-induced ventricular arrhythmia and compare them with those of conventional therapy alone. Methods: The study included 5 CPVT patients with a mutation in RYR2. They experienced episodic arrhythmic events despite conventional β-blocker therapy and were therefore given flecainide in addition. The effects of the addition of flecainide therapy on ventricular arrhythmia during exercise testing were compared with those of conventional therapy alone. Results: Both β-blockers alone and with additional flecainide increased the maximal workload attained at the onset of ventricular arrhythmia; however, only flecainide increased the sinus rate at the onset of ventricular arrhythmias. Furthermore, flecainide increased the exercise capacity by preventing exercise-induced arrhythmias. During a follow-up period of 17 ± 2 months, 1 patient experienced recurrent arrhythmic episodes that were associated with noncompliance. All patients reported improvements in their ability to perform the activities of daily living. Conclusion: Flecainide effectively reduced ventricular arrhythmias via a mechanism that differs from that of β-blockers in genotype-positive patients with CPVT. The specific effects of flecainide may be critical in the improvement noted in the patients' ability to perform daily activities. © 2013 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved.
  • Genetic screening of kCNJ8 in Japanese patients with J-wave syndromes or idiopathic ventricular fibrillation
    Qi Wang, Seiko Ohno, Koichi Kato, Megumi Fukuyama, Takeru Makiyama, Hiromi Kimura, Nobu Naiki, Mihoko Kawamura, Hideki Hayashi, Minoru Horie
    Journal of Arrhythmia 29(5) 261-264 2013年01月
    Background: J-point elevation has been demonstrated to be associated with ventricular fibrillation (VF) and has been proposed as a cause of the J-wave syndrome (JWS). A mutation of KCNJ8, S422L, was reported as a culprit gene. This study aimed to determine the prevalence of KCNJ8 mutations in a Japanese population with JWS or idiopathic VF (IVF). Methods: A total of 230 probands with JWS and IVF underwent genetic screening of KCNJ8. To analyze and compare clinical and electrocardiographic characteristics, the probands were divided into 4 groups: Brugada (Br) pattern only, early repolarization (ER) pattern only, Br and ER patterns, and true IVF. Results: The results of the genetic analysis revealed no S422L or other KCNJ8 mutations and indicated no significant difference between the groups. Conclusion: The KCNJ8 mutation showed no association with JWS or IVF among our Japanese patients. © 2013 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved.
  • Genetic basis of Brugada syndrome
    Minoru Horie, Seiko Ohno
    Journal of Arrhythmia 29(2) 71-76 2013年01月
    Brugada syndrome (BrS) is associated with the familial sudden death syndrome, and more than 10 genes have been reported as causative for or modifiers of BrS. All gene mutations are related to functional changes of inward sodium or calcium currents or outward potassium currents. SCN5A was the first gene known to be associated with BrS; it encodes the a-subunit of the cardiac sodium channel. Approximately 20% of BrS patients in genotyped cases were found to carry SCN5A mutations. The frequency for other BrS-associated gene mutations is so low that genotype-phenotype correlations for these genes have not been studied to the same extent as SCN5A-related BrS. In some families with SCN5A mutations, the penetrance of the mutations is low, and pathophysiological changes in the right ventricular outflow tract were reported in patients with SCN5A mutations. Furthermore, the phenotypes of SCN5A-related BrS can overlap with other phenotypes, including long QT and sick sinus syndrome, thereby suggesting that SCN5A mutations might be modifiers for BrS, but they do not direct cause BrS. Here, we summarize the genetic background of BrS, with a particular focus on recent progress in this field. © 2013 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved.
  • Letter by Hayashi et al regarding article, "early repolarization is an independent predictor of occurrences of ventricular fibrillation in the very early phase of acute myocardial infarctions"
    Hideki Hayashi, Minoru Horie
    Circulation: Arrhythmia and Electrophysiology 5(6) 114 2012年12月
  • High-risk long QT syndrome mutations in the Kv7.1 (KCNQ1) pore disrupt the molecular basis for rapid K+ permeation
    Don E. Burgess, Daniel C. Bartos, Allison R. Reloj, Kenneth S. Campbell, Jonathan N. Johnson, David J. Tester, Michael J. Ackerman, Véronique Fressart, Véronique Fressart, Isabelle Denjoy, Isabelle Denjoy, Pascale Guicheney, Pascale Guicheney, Arthur J. Moss, Seiko Ohno, Minoru Horie, Brian P. Delisle
    Biochemistry 51(45) 9076-9085 2012年11月
    Type 1 long QT syndrome (LQT1) is caused by loss-of-function mutations in the KCNQ1 gene, which encodes the K + channel (Kv7.1) that underlies the slowly activating delayed rectifier K + current in the heart. Intragenic risk stratification suggests LQT1 mutations that disrupt conserved amino acid residues in the pore are an independent risk factor for LQT1-related cardiac events. The purpose of this study is to determine possible molecular mechanisms that underlie the loss of function for these high-risk mutations. Extensive genotype-phenotype analyses of LQT1 patients showed that T322M-, T322A-, or G325R-Kv7.1 confers a high risk for LQT1-related cardiac events. Heterologous expression of these mutations with KCNE1 revealed they generated nonfunctional channels and caused dominant negative suppression of WT-Kv7.1 current. Molecular dynamics simulations of analogous mutations in KcsA (T85M-, T85A-, and G88R-KcsA) demonstrated that they disrupted the symmetrical distribution of the carbonyl oxygen atoms in the selectivity filter, which upset the balance between the strong attractive and K + -K + repulsive forces required for rapid K + permeation. We conclude high-risk LQT1 mutations in the pore likely disrupt the architectural and physical properties of the K + channel selectivity filter. © 2012 American Chemical Society.
  • Drug-induced QT-interval prolongation and recurrent torsade de pointes in a child with heterotaxy syndrome and KCNE1 D85N polymorphism
    Lisheng Lin, Hitoshi Horigome, Naoko Nishigami, Seiko Ohno, Minoru Horie, Ryo Sumazaki
    Journal of Electrocardiology 45(6) 770-773 2012年11月
    We present a child case of heterotaxy syndrome (asplenia syndrome) after Fontan procedure that showed extreme prolongation of QT interval and torsade de pointes (TdP) after administration of sodium channel blockers for paroxysmal atrial tachycardia. Despite low serum concentration of the drugs, QT prolongation persisted and TdP attacks with unconsciousness recurred, possibly in association with junctional bradycardia and myocardial damage although he had never experienced QT prolongation during bradycardia before. Temporal cardiac pacing via a venous route to exclude possible implication of bradycardia in induction of TdP was difficult to apply due to total cavopulmonary connection (TCPC) circulation. Continuous intravenous administration of low-dose isoproterenol was started but an appropriate heart rate for prevention of TdP was difficult to obtain. Finally, we were urged to conduct implantation of a DDD pacemaker combined with ICD surgically with epicardial leads, resulting in successful suppression of TdP and syncope. Screening of the genotype disclosed the KCNE1 D85N polymorphism, which is known as one of the typical disease-causing gene variants in long-QT syndrome (LQTS). © 2012 Elsevier Inc.
  • Agranulocytosis immediately after oral administration of cibenzoline and dabigatran in a patient with paroxysmal atrial fibrillation
    Hideki Hayashi Dr., Katsuyuki Kitoh, Kenichi Mitsunami, Minoru Horie
    Internal Medicine 51(15) 1987-1990 2012年08月
    This case report describes agranulocytosis immediately after oral administration of cibenzoline and dabigatran in a 70-year-old woman with paroxysmal atrial fibrillation (AF). No blasts were found in peripheral blood and bone marrow, and the white blood cell count increased abruptly by intravenous administration of granulocyte colony-stimulation factor, suggesting an allergic response caused by cibenzoline or dabigatran, or both. Though antiarrhythmic drugs with anticoagulation therapy are commonly used to treat paroxysmal AF, caution has to be paid to drug-induced agranulocytosis. © 2012 The Japanese Society of Internal Medicine.
  • Lipoprotein Particle Profiles by Nuclear Magnetic Resonance, Standard Lipids and Coronary Artery Calcification in a Japanese General Population: the Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA)
    第45回日本動脈硬化学会抄録 2013年
  • Using induced pluripotent stem cells to investigate cardiac phenotypes in Timothy syndrome
    Minora Horie
    Respiration and Circulation 60(5) 483-488 2012年05月
  • J-point elevation induced by double master two-step test
    Tomohide Yoshino, Hideki Hayashi, Ichiro Nakae, Minoru Horie
    Internal Medicine 51(14) 1941-1941 2012年07月
  • Prolonged ventricular asystole and acquired Brugada syndrome
    Minoru Horie, Yuko Nakazawa, Makoto Ito, Tomoya Ozawa
    Internal Medicine 51(13) 1799-1799 2012年07月
  • Phenotype variability in patients carrying KCNJ2 mutations
    Hiromi Kimura, Jun Zhou, Jun Zhou, Mihoko Kawamura, Hideki Itoh, Yuka Mizusawa, Wei Guang Ding, Jie Wu, Seiko Ohno, Takeru Makiyama, Akashi Miyamoto, Nobu Naiki, Qi Wang, Yu Xie, Tsugutoshi Suzuki, Shigeru Tateno, Yoshihide Nakamura, Wei Jin Zang, Makoto Ito, Hiroshi Matsuura, Minoru Horie
    Circulation: Cardiovascular Genetics 5(3) 344-353 2012年06月
    Background- Mutations of KCNJ2, the gene encoding the human inward rectifier potassium channel Kir2.1, cause Andersen-Tawil syndrome (ATS), a disease exhibiting ventricular arrhythmia, periodic paralysis, and dysmorphic features. However, some KCNJ2 mutation carriers lack the ATS triad and sometimes share the phenotype of catecholaminergic polymorphic ventricular tachycardia (CPVT). We investigated clinical and biophysical characteristics of KCNJ2 mutation carriers with "atypical ATS." Methods and Results- Mutational analyses of KCNJ2 were performed in 57 unrelated probands showing typical (≥2 ATS features) and atypical (only 1 of the ATS features or CPVT) ATS. We identified 24 mutation carriers. Mutation-positive rates were 75% (15/20) in typical ATS, 71% (5/7) in cardiac phenotype alone, 100% (2/2) in periodic paralysis, and 7% (2/28) in CPVT. We divided all carriers (n±45, including family members) into 2 groups: typical ATS (A) (n±21, 47%) and atypical phenotype (B) (n±24, 53%). Patients in (A) had a longer QUc interval [(A): 695±52 versus (B): 643±35 ms] and higher U-wave amplitude (0.24±0.07 versus 0.18±0.08 mV). C-terminal mutations were more frequent in (A) (85% versus 38%, P < 0.05). There were no significant differences in incidences of ventricular tachyarrhythmias. Functional analyses of 4 mutations found in (B) revealed that R82Q, R82W, and G144D exerted strong dominant negative suppression (current reduction by 95%, 97%, and 96%, respectively, versus WT at-50 mV) and T305S moderate suppression (reduction by 89%). Conclusions- KCNJ2 gene screening in atypical ATS phenotypes is of clinical importance because more than half of mutation carriers express atypical phenotypes, despite their arrhythmia severity. © 2012 American Heart Association, Inc.
  • Response to letter regarding article, "electrocardiographic characteristics and SCN5A mutations in idiopathic ventricular fibrillation associated with early repolarization"
    Hiroshi Watanabe, Akihiko Nogami, Kimie Ohkubo, Hiro Kawata, Yuka Hayashi, Taisuke Ishikawa, Takeru Makiyama, Satomi Nagao, Nobue Yagihara, Naofumi Takehara, Yuichiro Kawamura, Akinori Sato, Kazuki Okamura, Yukio Hosaka, Masahito Sato, Satoki Fukae, Masaomi Chinushi, Hirotaka Oda, Masaaki Okabe, Akinori Kimura, Koji Maemura, Ichiro Watanabe, Shiro Kamakura, Minoru Horie, Yoshifusa Aizawa, Wataru Shimizu, Naomasa Makita
    Circulation: Arrhythmia and Electrophysiology 5(2) 60-61 2012年04月
  • A connexin40 mutation associated with a malignant variant of progressive familial heart block type I
    Naomasa Makita, Akiko Seki, Naokata Sumitomo, Halina Chkourko, Shigetomo Fukuhara, Hiroshi Watanabe, Wataru Shimizu, Connie R. Bezzina, Can Hasdemir, Hideo Mugishima, Takeru Makiyama, Alban Baruteau, Estelle Baron, Minoru Horie, Nobuhisa Hagiwara, Arthur A.M. Wilde, Vincent Probst, Hervé Le Marec, Dan M. Roden, Naoki Mochizuki, Jean Jacques Schott, Mario Delmar
    Circulation: Arrhythmia and Electrophysiology 5(1) 163-172 2012年02月
    Background-Progressive familial heart block type I (PFHBI) is a hereditary arrhythmia characterized by progressive conduction disturbances in the His-Purkinje system. PFHBI has been linked to genes such as SCN5A that influence cardiac excitability but not to genes that influence cell-to-cell communication. Our goal was to explore whether nucleotide substitutions in genes coding for connexin proteins would associate with clinical cases of PFHBI and if so, to establish a genotype-cell phenotype correlation for that mutation. Methods and Results-We screened 156 probands with PFHBI. In addition to 12 sodium channel mutations, we found a germ line GJA5 (connexin40 [Cx40]) mutation (Q58L) in 1 family. Heterologous expression of Cx40-Q58L in connexin-deficient neuroblastoma cells resulted in marked reduction of junctional conductance (Cx40-wild type [WT] , 22.2 ± 1.7 nS, n=14; Cx40-Q58L, 0.56 ± 0.34 nS, n=14; P < 0.001) and diffuse localization of immunoreactive proteins in the vicinity of the plasma membrane without formation of gap junctions. Heteromeric cotransfection of Cx40-WT and Cx40-Q58L resulted in homogenous distribution of proteins in the plasma membrane rather than in membrane plaques in ̃ 50% of cells; well-defined gap junctions were observed in other cells. Junctional conductance values correlated with the distribution of gap junction plaques. Conclusions-Mutation Cx40-Q58L impairs gap junction formation at cell-cell interfaces. This is the first demonstration of a germ line mutation in a connexin gene that associates with inherited ventricular arrhythmias and emphasizes the importance of Cx40 in normal propagation in the specialized conduction system. © 2012 American Heart Association, Inc.
  • Successful catheter ablation of bidirectional ventricular premature contractions triggering ventricular fibrillation in catecholaminergic polymorphic ventricular tachycardia with RyR2 mutation
    Takashi Kaneshiro, Yoshihisa Naruse, Akihiko Nogami, Hiroshi Tada, Kentaro Yoshida, Yukio Sekiguchi, Nobuyuki Murakoshi, Yoshiaki Kato, Hitoshi Horigome, Mihoko Kawamura, Minoru Horie, Kazutaka Aonuma
    Circulation: Arrhythmia and Electrophysiology 5(1) 14-17 2012年02月
  • バイオマーカー
    蔦本 尚慶, 和田 直人, 山川 高哉, 伊部 邦宏, 酒井 宏, 河原 千穂, 堀江 稔
    日本内科学会雑誌 101(2) 345-353 2012年02月
    心不全診断・重症度評価・治療効果判定にバイオマーカーの果たす役割は大きい.今後,人口の高齢化に伴い心不全患者が増加し的確な診断と評価が重要になる.心不全は重症化すると予後不良であり,早期診断と治療が重要である.循環器疾患バイオマーカーの中でも,BNP,NT-proBNPは,慢性心不全ガイドラインにも述べられているように心不全の診断と評価に有用な心筋バイオマーカーであるが,腎機能など影響を及ぼす因子も考慮する必要がある.
  • Association of the use of proton pump inhibitors with adverse cardiovascular and bleeding outcomes after percutaneous coronary intervention in the Japanese real world clinical practice
    Takeshi Kimura, Takeshi Morimoto, Yutaka Furukawa, Yoshihisa Nakagawa, Kazushige Kadota, Masashi Iwabuchi, Satoshi Shizuta, Hiroki Shiomi, Tomohisa Tada, Junichi Tazaki, Yoshihiro Kato, Mamoru Hayano, Mitsuru Abe, Takashi Tamura, Manabu Shirotani, Shinji Miki, Mitsuo Matsuda, Mamoru Takahashi, Katsuhisa Ishii, Masaru Tanaka, Takeshi Aoyama, Osamu Doi, Ryuichi Hattori, Ryozo Tatami, Satoru Suwa, Akinori Takizawa, Yoshiki Takatsu, Masaaki Takahashi, Hiroshi Kato, Teruki Takeda, Jong Dae Lee, Ryuji Nohara, Chuwa Tei, Minoru Horie, Hirofumi Kambara, Hisayoshi Fujiwara, Kazuaki Mitsudo, Masakiyo Nobuyoshi, Toru Kita
    Cardiovascular Intervention and Therapeutics 26(3) 222-233 2011年12月
    Previous studies have shown inconsistent results regarding the effects of concomitant use of clopidogrel and proton pump inhibitors (PPI) on cardiovascular outcomes. We sought to evaluate the clinical impact of PPI-use in patients treated with thienopyridines after percutaneous coronary intervention (PCI) in a large Japanese observational database. Among 12446 patients discharged alive on thienopyridines (ticlopidine 90. 4% and clopidogrel 9. 6%), 3223 patients were treated with PPIs and 9223 patients without PPI at the time of hospital discharge. The PPI group included more patients with co-morbidities than the non-PPI group. The adjusted hazard ratio (HR) of PPI-use for a composite of cardiovascular death, myocardial infarction, and stroke was 1. 26 (95% confidence interval (CI) 1. 09-1. 47, p = 0. 002). The adjusted HR of PPI-use for bleeding was 1. 26 (95% CI 1. 05-1. 52, p = 0. 013). Cardiovascular and bleeding outcomes were not different among the three groups receiving three different types of PPI. The negative effect of PPI on cardiovascular outcome was consistently seen in both drug-eluting stent (DES) [HR 1. 31 (95% CI 1. 07-1. 6, p = 0. 0097)] and non-DES strata [HR 1. 25 (95% CI: 0. 99-1. 57, p = 0. 057)] (Interaction p = 0. 79) despite the fact that the duration of thienopyridine administration was significantly longer in patients receiving DES. In conclusion, cardiovascular outcomes after PCI were significantly worse in patients with PPI than in patients without PPI in the Japanese real clinical practice. However, the observed poorer cardiovascular outcome in patients receiving PPI was most likely to be related to residual confounding and seemed not causally related to attenuation of antiplatelet effect of thienopyridine through interaction with PPI. © 2011 Japanese Association of Cardiovascular Intervention and Therapeutics.
  • Letter by Hayashi et al Regarding Article, "Heritability of Early Repolarization: A Population-Based Study"
    Hideki Hayashi, Minoru Horie
    Circulation: Cardiovascular Genetics 4(5) 20 2011年10月
  • [108th Scientific Meeting of the Japanese Society of Internal Medicine: educational lecture: 3. Diagnosis and treatment of Japanese patients with Brugada syndrome].
    Minoru Horie
    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine 100 2599-2604 2011年09月
  • 致死性不整脈症候群の病態解明に関する研究 : 臨床・基礎研究(ヒト疾患特異的人工多能性幹(iPS)細胞を用いた解析)
    木村 剛, 北 徹, 堀江 稔
    医科学応用研究財団研究報告 31 447-454 2012年
  • KCNE5 (KCNE1L) variants are novel modulators of brugada syndrome and idiopathic ventricular fibrillation
    Seiko Ohno, Dimitar P. Zankov, Dimitar P. Zankov, Wei Guang Ding, Hideki Itoh, Takeru Makiyama, Takahiro Doi, Satoshi Shizuta, Tetsuhisa Hattori, Akashi Miyamoto, Nobu Naiki, Jules C. Hancox, Jules C. Hancox, Hiroshi Matsuura, Minoru Horie, Minoru Horie
    Circulation: Arrhythmia and Electrophysiology 4(3) 352-361 2011年06月
    Background-Brugada syndrome (BrS) has a significantly higher incidence among the male sex. Among genes coding ion channels and their modulatory proteins, KCNE5 (KCNE1L) is located in the X chromosome and encodes an auxiliary β-subunit for K channels. KCNE5 has been shown to modify the transient outward current (I to ), which plays a key role in determining the repolarization process in the myocardium. This study investigated whether KCNE5 mutations could be responsible for BrS and other idiopathic ventricular fibrillation (IVF). Methods and Results-In 205 Japanese patients with BrS or IVF who tested negative for SCN5A mutation, we conducted a genetic screen for KCNE5 variants. We identified 2 novel KCNE5 variants: p.Y81H in 3 probands and p.[D92E;E93X] in 1 proband from 4 unrelated families. Y81H was identified in 1 man and 2 women; D92E;E93X was found in a 59-year-old man. All probands received implantable cardioverter-defibrillators. Functional consequences of the KCNE5 variants were determined through biophysical assay using cotransfection with KCND3 or KCNQ1. In the experiments with KCND3, which encodes Kv4.3, I to was significantly increased for both KCNE5 variants compared to wild type. In contrast, there were no significant changes in current properties reconstructed by KCNQ1+wild type KCNE5 and the 2 variants. With the simulation model, both variants demonstrated notch-and-dome or loss-of-dome patterns. Conclusions-KCNE5 modulates I to , and its novel variants appeared to cause IVF, especially BrS, in male patients through gain-of-function effects on I to . Screening for KCNE5 variants is relevant for BrS or IVF. © 2011 American Heart Association, Inc.
  • 日本人一般男性における心疾患死亡リスクに対する早期再分極とn-3不飽和脂肪酸摂取量との交互作用の検討:NIPPON DATA80
    J Cardiol Jpn Ed(第60回日本心臓病学会抄録) -(-) 285-285 2012年
  • Microalbuminuria is associated with morning hypertension in hypertensive patients with glucose intolerance
    Shinji Tamaki, Yasuyuki Nakamura, Takeshi Kawashima, Jinya Matsui, Toshiyuki Kanamori, Minoru Horie
    Japanese Pharmacology and Therapeutics 39 209-215 2011年02月
    Objective: It is thought that morning blood pressure (BP) measurements at home are an important independent predictive factor of cerebrovascular and cardiovascular incidents. In addition, it is said that the appearance of microalbuminuria is a predictive factor of cardiovascular incidents. In this study, we investigated the association between microalbuminuria and morning BP at home. Methods: Subjects who had received medical treatment for hypertension in our outpatient clinic from October to December 2007 were enrolled. Of the 380 patients studied, which subjects gave informed consent for this study, 122 (32.1% ; 59 men, 63 women) showed glucose intolerance (fasting blood sugar (BS) ≧110 mg/dL and/or HbA1c≧5.8%) and 91 (41 men, 50 women) brought their home BP records to the outpatient clinic (74.6%). We examined the association between microalbuminuria and morning BP in these 91 patients. Results: There were 41 male patients (64.9±10.8 years old) and 50 female patients (67.0 ± 9.1 years old). Logistic analysis showed that age [odds ratio (OR) = 1.04 ; 95% confidence interval (CI) : 1.00-1.07 ; p < 0.01], SBP at the outpatient clinic (OR=0.94 ; 95%CI : 0.92-0.97 p < 0.01), sex (OR=0.96 ; 95%CI : 0.71-1.29 ; p=0.02) and microalbuminuria (OR= 1.69 ; 95%CI : 1.04-2.80 ; p < 0.01) were independent factors contributing to morning hypertension measurements at home. Conclusion: The contributing factors determining morning hypertension were : male gender, higher age, higher SBP at the outpatient clinic, and positive microalbuminuria. Microalbuminuria is known as a marker of disorders throughout the body. It is necessary to recommend more aggressive BP control for individuals with morning hypertension and glucose intolerance.
  • Carvedilol, a Non-Selective ß-with β-Blocker is Effective in Long QT Syndrome Type 2
    Hiromi Kimura, Yuka Mizusawa, Hideki Itoh, Akashi Miyamoto, Mihoko Kawamura, Tamiro Kawaguchi, Nobu Naiki, Yuko Oka, Seiko Ohno, Makoto Ito, Minoru Horie, Takeru Makiyama, Minoru Horie
    Journal of Arrhythmia 27(4) 324-331 2011年01月
    Background: β-blockers offer the first line therapy in congenital long QT syndrome (LQTS), and are more effective to prevent the cardiac event in LQTS type 1 than in type 2 or 3. In contrast, left cardiac sympathetic denervation (LCSD) was shown to be highly effective in patients refractory to β-blockers. Total sympathetic ablation by LCSD indicates the addititional involvement of “-adrenoceptor-mediated pathway. In genotyped LQT2 patients, we therefore hypothesized that blockade of “-adrenoceptor in addition to β-adrenoceptor by carvedilol could reduce cardiac events more efficiently than other types of β-blockers. Methods and Results: The study population consisted of 51 genotyped LQT2 patients (18 males, 23 ± 11 years old). They were divided into 2 groups (group 1: 43 patients treated with selective β-blockers, group 2: 8 patients with carvedilol) and retrospectively analyzed the efficacy of the respective β-blocker therapy in suppressing cardiac events. Cardiac events were observed in 11 patients of group 1 (26%) but none in group 2 during a follow-up period of 83 ± 80 months (P = 0.098). Conclusions: Carvedilol may be a potentially beneficial therapy for genotyped LQT2 patients who are refractory to other β selective blockers. © 2011, Japanese Heart Rhythm Society. All rights reserved.
  • Effect modification of dietary n-3 fatty acids on cardiovascular mortality risk by resting heart rate general population:NIPPON DATA80
    ESC2012 -(-) --- 2012年
  • 日本における Brugada 症候群 : 診断と治療
    堀江 稔
    日本内科学会雑誌 100(9) 2599-2604 2011年09月
  • KCNJ2変異を伴う Andersen-Tawil 症候群の神経生理所見
    定 翼, 国分 則人, 堀江 稔, 岡部 百佳, 駒ヶ嶺 朋子, 平田 幸一
    臨床神経生理学 : Japanese journal of clinical neurophysiology 39(1) 18-23 2011年02月
  • Mutations of KCNE Gene Family in Inherited Arrhythmia Syndromes
    Minoru Horie, Seiko Ohno, Jie Wu, Dimitar Zankov, Futoshi Toyoda, Wei Guang Ding, Hiroshi Matsuura
    journal of arrhythmia 27 244 2011年01月
    KCNE gene family consists of five different short genes encoding the regulatory proteins with a single transmembrane domain. The first member of the family (KCNE1) was cloned in 1988 (Takumi et al.) and was named as MinK because it reproduced slowly-activated voltage-gated K currents when expressed in Xenopus oocytes. Later in 1996, MinK (or KCNE1) has been shown to dramatically affect the expression of KCNQ1 channel, which is pore-forming subunit for human slow component of delayed rectifier K currents (IKS). Both are expressed in heart and inner ear. The reconstituted KCNE1/KCNQ1 channels display extremely slow activation and deactivation kinetics with enhanced current amplitude, which are much closer to those of human IKS. In contrast, another KCNE member (KCNE3) makes the channel constitutively open, and others reduce its amplitude or modulate gating. Interaction of KCNE family members with ion channels is very promiscuous. They drastically affect other pore-forming subunits of K channels such as KCNH2, KCNB1 (Kv2.1), KCND2 (Kv4.2) and KCND3 (Kv4.3). As they alter expression level, gating kinetics and second messenger regulation, their mutations may cause ion channelopathy through the malfunction of channels responsible for normal heart rhythm. In this symposium dedicated to Prof. Hiraoka, we would like to focus on these mutations in KCNE gene family and present several typical cases including our own experiences - KCNE1/KCNH2, KCNE2/KCND3, and KCNE3/KCNQ1. © 2011, Japanese Heart Rhythm Society. All rights reserved.
  • Clinical and Genetic Features of Japanese Patient with Congenital Long QT Syndrome
    Hisaki Makimoto, Takeshi Aiba, Shiro Kamakura, Yoshihiro Miyamoto, Wataru Shimizu, Minoru Horie, Satoshi Ogawa, Yoshifusa Aizawa, Tohru Ohe, Masakazu Yamgagishi, Naomasa Makita, Takeru Makiyama
    journal of arrhythmia 27 249 2011年01月
    Backgrounds: Genotype-phenotype aspects in Japanese patients (pts) with congenital long QT syndrome (LQTS) have not been fully elucidated. Methods and Results: Genotyped LQTS patients from Japanese multicenter registry (402 LQT1, 381 LQT2, and 113 LQT3 pts) were investigated. Age at first cardiac event (CE) was significantly lower and corrected QT (QTc) interval was significantly shorter in LQT1 than in LQT2 and LQT3 (13±14, 19±15, 17±20 yo; P=0.0004, 475± 46, 489±46, 482±58 ms; P=0.0003). Notched T wave (NTW) was more frequently observed in LQT2 (77%) than in LQT1 (9%) and LQT3 (10%). T wave alternance (TWA) was more frequently found in LQT3 (13%) compared with LQT1 (4%) and LQT2 (6%). Multivariate Cox-regression demonstrated that LQT1 and LQT2 pts with pore-site mutation and LQT3 pts with transmembrane mutation had significantly higher CE rate than those without (HR=1.52, 1.63, and 4.67, respectively). TWA (HR=2.37) in LQT1, longer QTc (HR=1.06 for QTc/10ms) and NTW (HR=1.51) in LQT2, and longer QTc (HR=1.11), NTW (HR=3.26), and TWA (HR=2.51) in LQT3 were independent risk factors of CE. Conclusions: In addition to mutations located in transmembrane region, some electrocardiographic parameters can be available as predictors of cardiac events in 3 genotypes of Japanese LQTS. © 2011, Japanese Heart Rhythm Society. All rights reserved.
  • A Weak Dominant Negative Mutation of KCNQ1-G269S Affects PKA-Mediated Up-Regulation of IKS Channels and Causes Adrenergic Triggered Long QT Syndrome
    Jie Wu, Nobu Naiki, Wei Guang Ding, Hiroshi Matsuura, Minoru Horie
    journal of arrhythmia 27 414 2011年01月
    Congenital Long QT Syndrome (LQTS) is an ion channelopathy characterized by QT interval prolongation in the ECG and ventricular tachyarrhythmias. It is caused by at least 13 types of gene mutations, among which the KCNQ1 gene mutation is most frequent and responsible for the LQT1. We identified a KCNQ1-G269S mutation in 11 patients from 4 families. Clinical data showed that most of patients were asymptomatic. Exercise stress test, however, prolonged their QTc intervals significantly. We engineered a G269S mutation by using PCR based mutagenesis and transfected into CHO or HEK293 cells together with KCNE1 by lipofectamine method. The whole cell IKS mutant currents were checked up using the patch-clamp technique. Co-expression of G269S decreased IKS currents in a mutant concentration-dependent manner, shifted the I-V relationship of IKS currents to more depolarizing direction, and accelerated the deactivation time of the currents. We found that G269S was a trafficking-refractory mutation and that the IKS reconstituted by G269A alone or the co-expression of wild type (WT) + G269S lost their response to β-adrenergic stimulation. Thus G269S mutation (1) exerted weak dominant-negative suppression effects on WT KCNQ1 channels; (2) coassembled with WT subunits to form tetramers and altered their gating kinetics and (3) may be associated with exercise-dependent unmasking of QTc prolongation. © 2011, Japanese Heart Rhythm Society. All rights reserved.
  • Long QT Syndromes Are Heterogeneous Disease Entities Presenting not only QT Prolongation but Multiple Phenotypes - Cases with Compound Heterozygous Mutations
    Minoru Horie, Hideki Itoh, Seiko Ohno, Takeru Makiyama, Wataru Shimizu, Shiro Kamakura, Kenshi Hayashi, Masakazu Yamagishi
    journal of arrhythmia 27 248 2011年01月
    Long QT syndromes (LQTS) consist of heterogeneous disease entities characterized by a remarkable prolongation of QT interval on ECG and a peculiar polymorphic ventricular tachycardia called “torsade de pointes”, which often degenerates into ventricular fibrillation and causing cardiogenic syncope or sudden death. Because of extensive studies on familial LQTS patients using the molecular genetics since early 1990s, it has been shown that genetic variants in genes encoding cardiac ion channels or their modulating proteins cause the delayed repolarization of ventricular action potential and thereby QT prolongation as a phenotype. Up to date, a variety of mutations in 13 different genes have been shown to be associated with LQTS. In the clinical setting, however, the first three subtypes (LQT1-3) are most frequently seen and presenting quite different phenotypes. Because the gene responsible for each subtype encodes a distinct ion current (I Ks , I Kr and I Na ), it is no wonder that the malfunction of specific channel leads to different clinical features. On a thorough screen for candidate genes in our multicenter study, in addition, we recognized that there were a substantial number of compound mutation cases (26 among 310 probands, 8.4%). In this symposium, we would like to make a brief overview on Japanese LQTS. © 2011, Japanese Heart Rhythm Society. All rights reserved.
  • Mutation Analysis of the KCNJ8 Gene in Japanese Patients with J-Wave Syndrome and Idiopathic Ventricular Fibrillation
    Wang Qi, Seiko Ohno, Takeru Makiyama, Hiromi Kimura, Nobu Naiki, Mihoko Kawamura, Koichi Kato, Minoru Horie
    journal of arrhythmia 27 415 2011年01月
    Background: Ventricular fibrillation (VF) is the most malignant arrhythmia causing the cardiac sudden death. Recently, the concept of J-wave syndrome (JWS), including the Brugada syndrome(BrS), has been proposed and early repolarization (J-point elevation) has been focused as one of clinical signs suggesting the primary electrical disease. A mutation of KCNJ8, S422L, was reported as the cause of JWS. In Japanese population with JWS or IVF, however, the prevalence of KCNJ8 mutations remains unknown. Method and Result: We screened KNCJ8 in 228 Japanese patients. They consisted of IVF patients with or without JWS (n=38) and asymptomatic JWS (mainly BrS, n=190), who were all negative for SCN5A mutation. The IVF group comprised 10 females and 28 males, and asymptomatic JWS group comprised 21 females and 169 males. In this cohort, we identified neither reported KCNJ8-S442L mutation nor other mutations including synonymous ones, using the denaturing high-performance liquid chromatography and the subsequent direct sequencing analysis. Conclusion: No KCNJ8 mutations were found in our Japanese IVF and asymptomatic JWS patients. Therefore KCNJ8 appears not to be the major gene responsible for IVF and asymptomatic JWS in Japan. © 2011, Japanese Heart Rhythm Society. All rights reserved.
  • Recent Advancement of Treatment in Catecholaminergic Polymorphic Ventricular Tachycardia
    Naokata Sumitomo, Wataru Shimizu, Hitoshi Horigome, Yoshihide Nakamura, Yoshio Arakaki, Harumizu Sakurada, Hiroshi Watanabe, Hiromitsu Nishizaki, Shiro Kamakura, Minoru Horie, Masayasu Hiraoka
    journal of arrhythmia 27 417 2011年01月
    Background: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is malignant arrhythmia characterized physical induced bidirectional or polymorphic ventricular tachycardia (VT). Methods and Results: From the Japanese registry of CPVT, 69 patients (M:F=25:44, age=11.7± 7.8years) were enrolled in this study. These patients were divided into 35 patients who were diagnosed during 1900s and 34 patients after 2000s. The incidence of sustained VT, nonsustained VT, and VF (10:22:3vs7:24:0, ns), the type of VT, and the rate of VT (194±29vs196±58, ns) were not different in these 2 groups. However, there was no sudden death in 2000s group, but 8 patients were died in 1900s group (p=0.003). Although statistically insignificant, there was no sudden death in 7 patients who was diagnosed over 20 year-old, however 8 of 62 patients were died who was diagnosed before 20 year-old. Conclusion: The prognosis of CPVT was markedly improved in the last 2 decade. This may be the result of propagation of the necessity of the restriction of exercise in the patients with CPVT, and also from the recent advancement of the use of antiarrhythmic medication, such as flecainide. The patients who were first diagnosed in adulthood may have better prognosis than the patients who were diagnosed in childhood. © 2011, Japanese Heart Rhythm Society. All rights reserved.
  • Site-Specific Arrhythmogenesis in Structurally Normal Heart of Non-Brugada Patients with Ventricular Arrhythmias Originating from Ventricular Outflow Tract
    Tomoya Ozawa, Makoto Ito, Hideki Itoh, Yuko Nakazawa, Yoshihisa Sugimoto, Takenori Yao, Akashi Miyamoto, Takashi Ashihara, Minoru Horie
    journal of arrhythmia 27 419 2011年01月
    Background: Ventricular fibrillation (VF) and/or polymorphic ventricular tachycardia (PVT) may be initiated by premature ventricular contractions (PVCs) from right ventricular outflow tract (RVOT). Methods: We evaluated the number and the location of PVCs/VTs foci of the 87 patients (mean age 43y, 54 females) who underwent radiofrequency ablation (RF) to the RVOT or coronary cusp without structural heart disease or Brugada syndrome. Results: Endocardial mapping showed no scar or low voltage area from RVOT during sinus rhythm. Seventy-five patients had monomorphic PVCs/VTs and exhibited no PVT or VF during both Holter monitors and RF. In 12 patients with PVCs of different morphologies, 9 patients had multiple PVCs originated from only RVOT septal area, and showed no PVT/VF. However, the other 3 patients had PVCs from both RVOT septum and free wall origins, and exhibited PVT and VF. Moreover, PVTs/VFs were triggered by spontaneous PVCs from only free wall foci of RVOT in those 3 patients. Conclusions: PVCs from free wall RVOT origin may induce malignant VT/VF in patients with idiopathic RVOT tachy-arrhythmias from multiple foci of both septal and free wall areas. Site-specific arrhythmogenesis presents in such patients. © 2011, Japanese Heart Rhythm Society. All rights reserved.
  • 第20回 心臓性急死研究会 就寝中に心室細動を発症した先天性QT延長症候群(LQT1)の1例
    松本 真, 小谷 英太郎, 吉田 博史, 堀江 格, 緒方 憲一, 田寺 長, 草間 芳樹, 新 博次, 堀江 稔
    心臓 40(3) 53-59 2008年
    症例は23歳,男性.既往歴,家族歴なし.午前7時ころ,就寝中に突然意識消失.救急隊が心室細動を確認,心肺蘇生を行いながら救命センターに搬送.低酸素脳症による視野狭窄を残すも低体温療法により全身状態改善,第22病日に精査目的で当科に転科.心肺蘇生直後の心電図では一過性に不完全右脚ブロック,V1,V2誘導のST上昇,QT延長(QTc 0,560秒)を認め,Brugada様心電図を認めたが経過とともにQTc 0.465秒に改善.血清電解質異常なし.心エコー図にて左右房室拡大なし,壁運動異常なし.冠動脈造影にて有意狭窄なし,アセチルコリン負荷試験陰性.LP陰性,TWAは陽性であった.電気生理学的検査で心室細動は誘発されず,Brugada症候群との鑑別のためピルジカイニド負荷試験を行うも陰性.以上より入院中に心室細動を来す原疾患を特定できなかったが,植込み型徐細動器植え込みを行った.後に遺伝子解析にてKCNQ1 W379Xの変異を認めLQT1と確定した.心室細動からの救命者で,確定診断に苦慮し遺伝子解析にてLQT1と確定し得たが,23歳で初発した就寝中の心室細動,およびW379Xの変異は従来の報告と異なりLQT1の非典型例と考えられた.
  • HEART's Selection 胸痛症候群の鑑別診断
    松本 鉄也, 堀江 稔
    心臓 40(7) 596-599 2008年
  • HEART's Selection 不整脈の遺伝子診断の歴史と変遷
    堀江 稔
    心臓 40(12) 1055-1059 2008年
  • Plasma brain natriuretic peptide as a useful biomarker of heart failure
    Takayoshi Tsutamoto, Minoru Horie
    Nippon Rinsho 4 417-425 2007年04月
  • A novel SCN5A mutation associated with the linker between III and IV domains of Nav1.5 in a neonate with fatal long QT syndrome
    Kenichiro Yamamura, Jun Muneuchi, Kiyoshi Uike, Kazuyuki Ikeda, Hirosuke Inoue, Yasushi Takahata, Yuichi Shiokawa, Yukako Yoshikane, Takeru Makiyama, Minoru Horie, Toshiro Hara
    International Journal of Cardiology 145(1) 61-64 2010年11月
  • Mutations of the Cardiac Ryanodine Recepter (RyR2) Gene in Catecholaminergic Polymorphic Ventricular Tachycardia
    Mihoko Kawamura, Iori Nagaoka, Kenichi Dohchi, Yukiko Nishio, Hideki Itoh, Hiromi Kimura, Akashi Miyamoto, Yuka Mizusawa, Yuko Jito, Katsuya Ishida, Makoto Ito, Takeru Makiyama, Seiko Ohno, Naokata Sumitomo, Kotaro Oyama, Minoru Horie
    journal of arrhythmia 27 187 2011年01月
    In 20cases with clinically-diagnosed catecholaminergic polymorphic ventricular tachycardia (CPVT) from 12 unrelated Japanese families, we conducted genetic testing on RyR2, a gene encoding the cardiac ryanodine receptor. The correlation between RyR2 - mutations and clinical phenotypes was investigated. The RyR2 mutations were found in 9 cases from the 20 probands (incidence: 45.0%) and in 3 from the 12 family members manifesting CPVT (incidence: 25.0%) Both bidirectional ventricular tachycardia (bVT) and atrial arrhythmias were Significantly more frequent in RyR2-positive compared to RyR2-negative CPVT patients. The fi ndings suggested that RyR2 mutations are closely related with bVT and atrial arrhythmias of early onset. © 2011, Japanese Heart Rhythm Society. All rights reserved.
  • Detection and prevalence of chronic obstructive pulmonary disease in a cardiovascular clinic: Evaluation using a hand held FEV1/FEV6meter and questionnaire
    Hiroshi Wada, Yasutaka Nakano, Taishi Nagao, Makoto Osawa, Hideto Yamada, Chikara Sakaguchi, Tetsuya Matsumoto, Takayoshi Tsutamoto, Makoto Ito, Minoru Horie
    Respirology 15 1252-1258 2010年11月
    Background and objective: COPD is one of the leading causes of morbidity and mortality worldwide, and its prevalence continues to increase. Although spirometry is indispensable for the diagnosis of COPD, other simple and reliable tools are necessary for screening of COPD because spirometry is not widely available. This study investigated the usefulness of a combination of an electronic FEV 1 /FEV 6 meter (PiKo-6) with a COPD questionnaire as a screening method in patients with cardiovascular diseases. Methods: The PiKo-6 and the COPD questionnaire of the International Primary Care Airways Group were used to screen patients attending a cardiovascular outpatient clinic. Patients with FEV 1 /FEV 6 < 70% were defined as having airflow limitation. Patients diagnosed with airflow limitation underwent spirometry. Using data from the PiKo-6 and the COPD questionnaire, patients were assigned to a COPD group or a non-COPD group. The relationship between PiKo-6 measurements and spirometry was also evaluated. Results: Among 753 patients, 82 (10.9%) showed airflow limitation when assessed with the PiKo-6. Of these patients, 79 (10.5%) were assigned to the COPD group. FEV 1 , FEV 6 and FEV 1 /FEV 6 , as measured with the PiKo-6, correlated significantly with FEV 1 , FVC and FEV 1 /FVC, respectively, as measured by spirometry (r=0.865, 0.751 and 0.57). Among the cardiovascular comorbidities, heart failure and ischaemic heart disease showed slightly stronger associations with airflow limitation (13.8% and 12.5%, respectively). Conclusions: Combination of the PiKo-6 with a COPD questionnaire may be a useful and feasible method of identifying undiagnosed COPD patients attending a cardiovascular outpatient clinic. This study shows for the first time that the combination of an electronic, hand held FEV 1 /FEV 6 meter with a COPD questionnaire is a useful and feasible method for identifying undiagnosed COPD among patients with cardiovascular diseases attending a cardiovascular outpatient clinic. © Asian Pacific Society of Respirology.
  • Ventricular Fibrillation Triggered during Radiofrequency Energy Delivery for Verapamil-Sensitive Idiopathic Left Ventricular Tachycardia
    Tomoya Ozawa, Makoto Ito, Yuko Nakazawa, Takashi Ashihara, Akashi Miyamoto, Minoru Horie, Yoshihisa Sugimoto, Takenori Yao
    journal of arrhythmia 27 208 2011年01月
    Verapamil-sensitive idiopathic left ventricular tachycardia (VT) can be suppressed by radiofrequency ablation (RF) on the Purkinje network. RF delivered on the Purkinje fi bers triggers premature ventricular contractions or repetitive ventricular response and disappear after cessation of RF. We present a case with idiopathic left VT who represented ventricular fibrillation (VF) during RF on the Purkinje network. Case: A 15-year-old male admitted our hospital because of recurrent sustained VT with QRS morphology of right bundle branch block and left axis deviation. Intravenous verapamil terminated VT. However, electrophysiologic study could not induce VT even if isoproterenol infusion. We delivered RF energy at the distal left posterior fascicular region where Purkinje potentials were recorded during sinus rhythm with pace-mapping QRS morphology mimicking VT-QRS. Shortly after RF delivery, polymorphic VT induced and degenerated into VF. RF deliveries around the VF site induced similar responses. Then, we created RF lesions on the Purkinje fibers more proximal to the VF-induced sites. No VT was documented 3 years after ablation. Conclusion: Purkinje network appears to have potential role for VF induction. RF ablations at the proximal site of the critical Purkinje network can prevent VT/VF occurrence in such case. © 2011, Japanese Heart Rhythm Society. All rights reserved.
  • Effect of eplerenone versus spironolactone on cortisol and hemoglobin A1c levels in patients with chronic heart failure
    Masayuki Yamaji, Takayoshi Tsutamoto, Chiho Kawahara, Keizo Nishiyama, Takashi Yamamoto, Masanori Fujii, Minoru Horie
    American Heart Journal 160(5) 915-921 2010年11月
    Background: It has been reported that mineralocorticoid receptor antagonist improves the prognosis of chronic heart failure (CHF). Recently, hemoglobin A1c (HbA 1c ) levels have been reported to be an independent risk factor for mortality in CHF, suggesting the important role of insulin resistance in CHF. We compared the metabolic effect of a selective mineralocorticoid receptor blocker eplerenone with spironolactone in CHF patients. Methods: One hundred seven stable outpatients with mild CHF, who were already receiving standard therapy for CHF, were randomized (1:2) to spironolactone (25 mg/d) or eplerenone (50 mg/d). Plasma levels of B-type natriuretic peptide, adiponectin, HbA 1c and cortisol were measured before and after 4 months treatment with spironolactone or eplerenone. Results: There were no differences in baseline characteristics including hemodynamic parameters and plasma levels of biomarkers between 2 groups. In both groups, plasma B-type natriuretic peptide levels were significantly decreased and plasma aldosterone levels were significantly increased after 4 months. In patients receiving spironolactone (n = 34), plasma adiponectin levels were significantly decreased (12.6 ± 1.4-11.2 ± 1.3 μg/mL, P < .0001) and HbA 1c and cortisol levels were significantly increased (5.61 ± 0.1-5.8 ± 0.1%, P < .0001, 11.3 ± 0.8-14.7 ± 1.3 μg/dL, P = .003, respectively). In patients receiving spironolactone, there was a significant positive correlation between the change in cortisol and the change in HbA 1c (r = 0.489, P = .003). In contrast, in patients receiving eplerenone (n = 73), plasma levels of adiponectin, HbA 1c and cortisol did not change. Conclusion: These findings indicated that the metabolic effect of eplerenone differed from that of spironolactone and that eplerenone had a superior metabolic effect especially on HbA 1c in CHF patients. © 2010 Mosby, Inc.
  • 6.包括的管理・治療 5.アテローム血栓症を有する外来患者における1年追跡による循環器イベント発生率の検討(REACH Registry)
    血栓と循環 19(3) 219-221 2011年
  • カテコラミン誘発性多形性心室頻拍を疑う患者における遺伝子変異の検討 : 心筋リアノジン受容体について
    川村 美朋子, 長岡 伊織, 道智 賢市, 西尾 由貴子, 伊藤 英樹, 木村 紘美, 宮本 証, 水澤 有香, 地藤 優子, 石田 勝也, 伊藤 誠, 牧山 武, 大野 聖子, 住友 直方, 小山 耕太郎, 堀江 稔
    心電図 = Electrocardiology 30(4) 298-305 2010年10月
    本研究は,臨床的にカテコラミン誘発性多形性心室頻拍(CPVT)が疑われる20例とその家族12例を対象に,心筋リアノジン受容体(RyR2)の遺伝子解析を行った.またRyR2遺伝子異常の有無による臨床症状の相違について検討した.発端者20例のうち9例(同定率:45.0%),家族12例のうち3例(同定率:25.0%)においてRyR2の遺伝子変異を認めた.
    RyR2変異を認めたCPVT患者には二方向性心室頻拍(bVT)が有意に多く(感度:77%,特異度:72%),QT間隔の延長のないQT延長症候群(特にtype1)との区別に有用と考えられた.またRyR2の遺伝子変異を有するCPVT患者において心房不整脈が有意に認められ,RyR2と若年性の心房不整脈の関与が示唆された.
  • 高血圧と不整脈--高血圧の治療によって不整脈発症の予防は可能か? (特集 ライフスタイルと不整脈のかかわりを探る)
    堀江 稔
    Life style medicine 4(4) 322-326 2010年10月
  • P wave and the development of atrial fibrillation
    Katsuya Ishida, Hideki Hayashi, Akashi Miyamoto, Yoshihisa Sugimoto, Makoto Ito, Yoshitaka Murakami, Minoru Horie
    Heart Rhythm 7(3) 289-294 2010年03月
    Background: Terminal P-wave inversion in lead V 1 representing left atrial overload has been considered a precursor of atrial fibrillation (AF). Objective: The purpose of this study was to determine whether this P-wave morphologic characteristic can predict the development of AF. Methods: Digital analysis of 12-lead ECGs was performed to enroll patients with P terminal force ≥0.06 s × 2 mm in lead V 1 from among a database of 308,391 ECG recordings. The prognostic value of ECG characteristics for developing AF was determined. Results: A total of 78 patients (mean age 52 ± 19 years) with left atrial overload were chosen from among 102,065 patients in the database. During mean follow-up of 43 months, 15 (19%) patients developed AF (AF group) versus 63 (81%) patients who did not (non-AF group). No significant difference was noted between the AF and non-AF groups with regard to the area, duration, and amplitude of the P-wave terminal portion in lead V 1 . In contrast, the area, duration, and amplitude of the P-wave initial portion in the same lead were significantly greater in the AF group than in the non-AF group (114.6 ± 73.0 μV × ms vs 73.1 ± 59.3 μV × ms, 42.2 ± 12.4 ms vs 35.7 ± 10.1 ms, and 94.0 ± 39.9 μV vs 68.8 ± 49.4 μV, respectively; P < .05 for each). Multivariate analysis confirmed that the area of the P-wave initial portion was independently associated with the development of AF (hazard ratio 4.02, 95% confidence interval 1.25-17.8; P = .018). Conclusion: P-wave initial portion in lead V 1 was an independent risk stratifier of AF development in patients with marked left atrial overload. © 2010 Heart Rhythm Society.
  • 遺伝性不整脈の診断と治療におけるiPS細胞利用の可能性 (臨床遺伝子学'10)
    堀江 稔
    最新医学 65(0) 2095-2101 2010年09月
  • Dose-dependent prognostic effect of carvedilol in patients with chronic heart failure: Special reference to ranscardiac gradient of norepinephrine (Circulation Journal (2009), 73, (2270-2275))
    Keizo Nishiyama, Takayoshi Tsutamoto, Masayuki Yamaji, Chiho Kawahara, Takashi Yamamoto, Masanori Fujii, Minoru Horie
    Circulation Journal 74(2) 385 2010年02月
  • QT短縮症候群 (第1土曜特集 ここまで進んだ 不整脈研究の最新動向) -- (心室細動をめぐる新展開)
    堀江 稔
    医学のあゆみ 234(6) 719-722 2010年08月
  • 肺静脈隔離術後の心房細動再発検出における携帯型心電計の有用性
    中澤 優子, 芦原 貴司, 八尾 武憲, 城 日加里, 伊藤 英樹, 杉本 喜久, 伊藤 誠, 堀江 稔
    心電図 = Electrocardiology 30 "S-1-7" 2010年05月
  • 心電学研究の進歩(循環器学2009年の進歩)
    堀江 稔
    循環器専門医 : 日本循環器学会専門医誌 18(1) 90-95 2010年03月
  • 座談会「循環器病学の将来展望--基礎と臨床の融合」 iPS細胞利用の心筋再生などに期待--循環器疾患各領域で画期的な治療法開発が進む
    北 徹, 澤 芳樹, 堀江 稔
    MD 7(1) 8-17 2010年01月
  • 遺伝子異常と不整脈 (特集 危険な不整脈--みきわめ方と正しい対応)
    伊藤 英樹, 堀江 稔
    臨牀と研究 87(1) 98-101 2010年01月
  • 座談会 冠動脈疾患の治療を考える~JSHガイドライン改正を受けて~
    血圧 17 35-40 2010年
  • 肺静脈隔離手術後の心房細動再発検出における携帯型心電機の有用性。
    心電図 30(S-1) 71 2010年
  • Effect of carperitide on plasma adiponectin levels in acute decompensated heart failure patients with diabetes mellitus
    Masayuki Yamaji, Takayoshi Tsutamoto, Toshinari Tanaka, Chiho Kawahara, Keizo Nishiyama, Takashi Yamamoto, Masanori Fujii, Minoru Horie
    Circulation Journal 73(12) 2264-2269 2009年12月
    Background: It is reported that adiponectin has a cardioprotective effect and is decreased in type 2 diabetes mellitus (DM). Methods and Results: The effect of carperitide (atrial natriuretic peptide: ANP) on plasma adiponectin levels was evaluated in acute decompensated heart failure (ADHF) patients with and without DM. In 47 patients (DM: n= 11) who were admitted with ADHF, blood samples were collected before and 7 days after administration of carperitide. The plasma levels of ANP, brain natriuretic peptide (BNP), aldosterone and adiponectin were measured. Plasma adiponectin levels were significantly increased (17.6±1.5 to 19.6±1.8μg/ml, P=0.0003) concomitant with the increase in ANP and decrease in BNP 7 days after carperitide infusion. Although adiponectin levels before treatment were slightly lower in ADHF patients with DM, the % increase in adiponectin levels was significantly greater in ADHF patients with DM than in those without DM (26.7 vs 6.6%, P=0.007). In the stepwise multi-variate analyses, a higher plasma aldosterone levels before treatment (P=0.04) and DM (P=0.01) were significant independent predictors of a greater % increase in adiponectin levels after treatment with carperitide. Conclusions: Carperitide infusion increases the plasma adiponectin level, especially in ADHF patients with DM.
  • 先天性QT延長症候群の遺伝子診断―複数異変症例の検討―
    伊藤英樹, 清水渉, 林研至, 山形研一郎, 坂口知子, 大野聖子, 牧山武, 赤尾昌治, 藍智彦, 野田崇, 宮崎文, 宮本恵宏, 山岸正和, 鎌倉史郎, 堀江稔
    心電図 30(3) 195-199 2010年
  • Effect of carvedilol on plasma adiponectin concentration in patients with chronic heart failure: Reply
    Masayuki Yamaji, Takayoshi Tsutamoto, Toshinari Tanaka, Keizo Nishiyama, Chiho Kawahara, Masanori Fujii, Takashi Yamamoto, Minoru Horie
    Circulation Journal 73(12) 2364 2009年12月
  • 家族性ペースメーカー植え込み症例における遺伝的背景の検討―心臓Na+チャネル病、LaminA/C遺伝子関連心筋症―
    牧山武, 静田聡, 赤尾昌治, 木村剛, 堀江稔
    心電図 30(3) 200-208 2010年
  • Long-term prognosis of probands with brugada-pattern ST-elevation in leads V 1-V 3
    Shiro Kamakura, Tohru Ohe, Kiyoshi Nakazawa, Yoshifusa Aizawa, Akihiko Shimizu, Minoru Horie, Satoshi Ogawa, Ken Okumura, Kazufumi Tsuchihashi, Kaoru Sugi, Naomasa Makita, Nobuhisa Hagiwara, Hiroshi Inoue, Hirotsugu Atarashi, Naohiko Aihara, Wataru Shimizu, Takashi Kurita, Kazuhiro Suyama, Takashi Noda, Kazuhiro Satomi, Hideo Okamura, Hitonobu Tomoike
    Circulation: Arrhythmia and Electrophysiology 2(5) 495-503 2009年10月
    Background-The prognosis of patients with saddleback or noncoved type (non-type 1) ST-elevation in Brugada syndrome is unknown. The purpose of this study was to clarify the long-term prognosis of probands with non-type 1 ECG and those with coved (type 1) Brugada-pattern ECG. Methods and Results-A total of 330 (123 symptomatic, 207 asymptomatic) probands with a coved or saddleback ST-elevation ≥1 mm in leads V 1 -V 3 were divided into 2 ECG groups-type 1 (245 probands) and non-type 1 (85 probands)-and were prospectively followed for 48.7≥15.0 months. The absence of type 1 ECG was confirmed by drug provocation test and multiple recordings. The ratio of individuals with a family history of sudden cardiac death (14%) was lower than previous studies. Clinical profiles and outcomes were not notably different between the 2 groups (annual arrhythmic event rate of probands with ventricular fibrillation; type 1: 10.2%, non-type 1: 10.6%, probands with syncope; type 1: 0.6%, non-type 1: 1.2%, and asymptomatic probands; type 1: 0.5%, non-type 1: 0%). Family history of sudden cardiac death at age < 45 years and coexistence of inferolateral early repolarization with Brugada-pattern ECG were independent predictors of fatal arrhythmic events (hazard ratio, 3.28; 95% confidence interval, 1.42 to 7.60; P=0.005; hazard ratio, 2.66; 95% confidence interval, 1.06 to 6.71; P=0.03, respectively, by multivariate analysis), although spontaneous type 1 ECG and ventricular fibrillation inducibility by electrophysiological study were not reliable parameters. Conclusions-The long-term prognosis of probands in non-type 1 group was similar to that of type 1 group. Family history of sudden cardiac death and the presence of early repolarization were predictors of poor outcome in this study, which included only probands with Brugada-pattern ST-elevation. (Circ Arrhythmia Electrophysiol. 2009;2:495-503.) Copyright © 2009 American Heart Association, Inc.
  • ペースメーカ植込み同胞例に認められたあらたなLamin A/C変異A novel lamin A/C gene mutation in siblings treated with cardiac pacemaker.
    心電図 31(1) 18-24 2010年
  • Prevalence of atrial fibrillation in the general population of Japan: An analysis based on periodic health examination
    Hiroshi Inoue, Akira Fujiki, Hideki Origasa, Satoshi Ogawa, Ken Okumura, Isao Kubota, Yoshifusa Aizawa, Takeshi Yamashita, Hirotsugu Atarashi, Minoru Horie, Tohru Ohe, Yoshinori Doi, Akihiko Shimizu, Akiko Chishaki, Tetsunori Saikawa, Katsusuke Yano, Akira Kitabatake, Hideo Mitamura, Itsuo Kodama, Shiro Kamakura
    International Journal of Cardiology 137(2) 102-107 2009年10月
    Background: The mortality and morbidity rates of various cardiovascular diseases differ between Western countries and Japan. The age- and gender-specific prevalence rate of atrial fibrillation (AF) in the general population of Japan was determined using the data from periodic health examinations in 2003. Methods: Data of 630,138 subjects aged 40 years or more (47% were men and 34% were employees of companies and local governments) were collected from northern to southern Japan. The prevalence of diagnosed AF in each 10-year age group of both men and women was determined. Based on these prevalence rates and the Registry of Residents, the number of people having AF in Japan was estimated. Results: The prevalence rate of AF increased as both male and female subjects aged, and it was 4.4% for men but only 2.2% for women aged 80 years or more (p < 0.0001). As a whole, the AF prevalence of men was three times that of women (1.35 versus 0.43%, p < 0.0001). There may be approximately 716,000 people (95% confidence interval (CI), 711,000-720,000) with AF in Japan, an overall prevalence of 0.56%. The number of people having AF was projected to be 1.034 (95% CI, 1.029-1.039) million, an overall prevalence of 1.09%, in 2050. Conclusions: The prevalence of AF increased in Japan as the population aged, as in Western countries. The overall prevalence of AF in Japan is approximately two-thirds of that in the USA. The projected increase in the number of people having AF is modest in Japan in 2050. © 2008 Elsevier Ireland Ltd. All rights reserved.
  • 学会レポート 第27回日本心電学会学術集会
    心電図 30 432-439 2010年
  • Left ventricular involvement in arrhythmogenic right ventricular cardiomyopathy demonstrated by multidetector-row computed tomography.
    Shinro Matsuo, Yuichi Sato, Ichiro Nakae, Daisuke Masuda, Makiko Yomota, Takashi Ashihara, Minoru Horie
    Int J Cardiol  115(3) 129-131 2007年02月
    Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a condition in which the right ventricle is partially or totally replaced by the adipose tissue. Pathological abnormalities affect the left ventricle as well as the right ventricle, particularly the epimyocardium. Multidetector-row computed tomography, which allowed excellent visualization of not only the coronary arteries but also the myocardium with submillimeter spatial resolution and high signal-to-noise ratio, would be more suitable for the assessment of the extent of adipose tissue involvement in the right and left ventricular myocardium. We present a patient who was diagnosed as having ARVC with left ventricular involvement and underwent cardioverter defibrillator implantation. © 2006 Elsevier Ireland Ltd. All rights reserved.
  • Cardioverter defibrillator implantation in a patient with double chambered right ventricle.
    Shinro Matsuo, Yuichi Sato, Ichiro Nakae, Yuko Oka, Minoru Horie
    Int J Cardiovasc Imaging 23(4) 459-462 2007年08月
    Double-chambered right ventricle (DCRV) is a rare form of congenital heart disease in which the right ventricle is divided into a high-pressure inlet site and a low-pressure outlet site by anomalous muscle bands. We describe a patient with DCRV presenting with ventricular tachycardia. © Springer Science+Business Media, Inc. 2006.
  • Depiction of a new pulmonary vein variant using multidetector-row computed tomography.
    Shinro Matsuo, Yuichi Sato, Ichiro Nakae, Daisuke Masuda, Tetsuya Matsumoto, Minoru Horie
    Cardiovasc Revasc Med 8(3) 207-208 2007年07月
  • Cholesteryl Ester Transfer Protein, Coronary Calcium, and Intima-Media Thickness of the Carotid Artery in Middle-Age Japanese Men
    Tomonori Okamura, Tomonori Okamura, Akira Sekikawa, Takashi Kadowaki, Aiman El-Saed, Robert D. Abbott, J. David Curb, Daniel Edmundowicz, Yasuyuki Nakamura, Kiyoshi Murata, Atsunori Kashiwagi, Kim Sutton-Tyrrell, Rhobert W. Evans, Joseph M. Zmuda, Hiroshi Maegawa, Atsushi Hozawa, Ken Ichi Mitsunami, Yoshihiko Nishio, Iva Miljkovic-Gacic, Minoru Horie, Naomi Miyamatsu, Yoshitaka Murakami, Lewis H. Kuller, Hirotsugu Ueshima
    American Journal of Cardiology 104(6) 818-822 2009年09月
    The relation between cholesteryl ester transfer protein (CETP) levels and atherosclerosis is controversial. We examined whether the serum CETP levels were associated with subclinical atherosclerosis, independent of its most common gene variant, in a sample of Japanese men. A population-based cross-sectional study of 250 Japanese men aged 40 to 49 years was conducted to assess the intima-media thickness of the carotid artery, coronary artery calcium, serum CETP levels, and the CETP D442G gene variant. Compared with the lowest CETP quartile, the multivariate adjusted odds ratio for coronary artery calcium was 0.77 (95% confidence i nterval 0.18 to 3.36), 0.96 (95% confidence interval 0.27 to 3.40), and 3.49 (95% confidence interval 1.05 to 11.6) with increasing CETP quartiles. The serum CETP quartiles were also positively associated with the intima-media thickness of the carotid artery (adjusted mean 602, 616, 615, and 646 μm for the lowest to top quartile, respectively). The findings remained unchanged after additional adjustment for the CETP D442G gene variant. No significant difference was found in the prevalence of coronary artery calcium or in the mean intima-media thickness of the carotid artery between participants with and without the CETP D442G gene variant. © 2009 Elsevier Inc. All rights reserved.
  • A novel clinical indicator using Tc-99m sestamibi for evaluating cardiac mitochondrial function in patients with cardiomyopathies.
    Shinro Matsuo, Ichiro Nakae, Takayoshi Tsutamoto, Noriake Okamoto, Minoru Horie
    J Am Coll Cardiol 49(9) 61A-62A-220 2007年04月
    Background: Technetium 99m sestamibi (MIBI) is a technetium-labeled myocardial perfusion agent that is taken up by the myocardial cell in proportion to myocardial regional blood flow and remains fixed in the myocardial cell over a long period of time. Previous studies have suggested that MIBI shows very slow myocardial clearance after its initial uptake in an animal model, which is related to mitochondrial function. This study was designed to test the hypothesis that MIBI washout can be used to evaluate the severity of congestive heart failure in comparison to other clinical parameters in patients with cardiomyopathies. Methods and Results: After administration of MIBI, 61 patients with nonischemic congestive heart failure (49 with dilated cardiomyopathy and 12 with other cardiomyopathies) and 7 normal control subjects were examined by electrocardiography-gated myocardial perfusion single photon emission computed tomography and planar data acquisition in the early and delayed phases (interval of 3 hours). Myocardial MIBI washout rates were calculated from the early and delayed planar images. Left ventricular function (systolic and diastolic) was analyzed by use of QGS data. Plasma levels of B-type natriuretic peptide and iodine 123 metaiodobenzylguanidine (MIBG) parameters were also measured. Patients were followed up for a mean of 12 months (range, 1-19 months). As the severity of the New York Heart Association (NYHA) functional class advanced, the washout rate of MIBI increased (21.6% ± 2.4% in those with NYHA class I [n = 23], 28% ± 4% in those with NYHA class II [n = 27] , and 35% ± 5% in those with NYHA class III [n = 10]; P < .05, analysis of variance). The washout rate of MIBI was positively correlated with the level of B-type natriuretic peptide (r = 0.31, P < .05), end-diastolic volume (r = 0.396, P < .01), and end-systolic volume (r = 0.496, P < .01) and was negatively correlated with left ventricular ejection fraction (r = 0.523, P < .01), peak filling rate (r = 0.444, P < .01), and first-third ejection fraction (r = 0.414, P < .01). The parameters of MIBG scintigraphy were calculated as the heart-mediastinum count ratio (1.9 ± 3) and washout rate (38% ± 4%). We found a significant relationship between the washout rate of MIBI and the heart-mediastinum count ratio of MIBG (r = 0.51, P < .01). Patients with a higher washout rate of MIBI had a higher cardiac event rate (≥28%) than those with a lower washout rate ( < 28%) (P < .05). Conclusions: The myocardial washout rate of MIBI is thought to be a novel marker for the diagnosis of myocardial damage or dysfunction, providing prognostic information in patients with congestive heart failure. © 2007 American Society of Nuclear Cardiology.
  • Angiotensin II type 1 receptor mediates partially hyposmotic-induced increase of i Ks current in guinea pig atrium
    Dimitar P. Zankov, Futoshi Toyoda, Mariko Omatsu-Kanbe, Hiroshi Matsuura, Minoru Horie
    Pflugers Archiv European Journal of Physiology 458(5) 837-849 2009年09月
    A repolarizing conduction in the heart augmented by hyposmotic or mechanically induced membrane stretch is the slow component of delayed rectifier K + current (I Ks ). I Ks upregulation is recognized as a factor promoting appearance of atrial fibrillation (AF) since gain-of-function mutations of the channel genes have been detected in congenital AF. Mechanical stretch activates angiotensin II type 1 (AT 1 ) receptor in the absence of its physiological ligand angiotensin II. We investigated the functional role of AT 1 receptor in I Ks enhancement in hyposmotically challenged guinea pig atrial myocytes using the whole-cell patch-clamp method. In atrial myocytes exposed to hyposmotic solution with osmolality decreased to 70% of the physiological level, I Ks was enhanced by 84.1%, the duration of action potential at 90% repolarization (APD 90 ) was decreased by 16.8%, and resting membrane potential was depolarized (+4.9 mV). The hyposmotic-induced effects on I Ks and APD 90 were significantly attenuated by specific AT 1 receptor antagonist candesartan (1 and 5∈μM). Pretreatment of atrial myocytes with protein tyrosine kinase inhibitors tyrphostin A23 and A25 suppressed but the presence of tyrosine phosphatase inhibitor orthovanadate augmented hyposmotic stimulation of I Ks . The above results implicate AT 1 receptor and tyrosine kinases in the hyposmotic modulation of atrial I Ks and suggest acute antiarrhythmic properties of AT 1 antagonists in the settings of stretch-related atrial tachyarrhythmias. © 2009 Springer-Verlag.
  • A novel KCNH2 mutation as a modifier for short QT interval
    Hideki Itoh, Tomoko Sakaguchi, Takashi Ashihara, Wei Guang Ding, Iori Nagaoka, Yuko Oka, Yuko Nakazawa, Takenori Yao, Hikari Jo, Makoto Ito, Kazufumi Nakamura, Tohru Ohe, Hiroshi Matsuura, Minoru Horie
    International Journal of Cardiology 137(1) 83-85 2009年09月
    In a 34-year-old man showing short QT interval (QTc 329 ms), we identified a novel C-terminal KCNH2 mutation, R1135H. Using a heterologous expression system with CHO cells, the mutant channels were found to display a significantly slow deactivation, which resulted in a gain-of-function for reconstituted 'I Kr ' channels. This mutation could modify clinical phenotypes for this patient. © 2008 Elsevier Ireland Ltd. All rights reserved.
  • QT延長の潜在的危険性の予知 : 遺伝子多型:KCNE1-D85N(4.バイオマーカー・遺伝子多型とリスク評価,<特集>第73回日本循環器学会学術集会)
    西尾 由貴子, 堀江 稔
    循環器専門医 : 日本循環器学会専門医誌 17(2) 237-242 2009年09月
  • Coronary risk factor profile and prognostic factors for young Japanese patients undergoing coronary revascularization
    Yutaka Furukawa, Yutaka Furukawa, Natsuhiko Ehara, Ryoji Taniguchi, Yoshisumi Haruna, Neiko Ozasa, Naritatsu Saito, Takahiro Doi, Kozo Hoshino, Toshihiro Tamura, Satoshi Shizuta, Mitsuru Abe, Masanao Toma, Takeshi Morimoto, Takeshi Morimoto, Satoshi Teramukai, Satoshi Teramukai, Masanori Fukushima, Masanori Fukushima, Toru Kita, Takeshi Kimura, Takeshi Kimura, Jong Dae Lee, Kuniyoshi Tanaka, Katsuo Okazaki, Masaaki Takahashi, Teiji Oda, Shigeo Matsui, Naohiro Ohashi, Eiichi Matsuyama, Makoto Kadoya, Yoshiki Takatsu, Shinichi Nomoto, Kazuaki Kataoka, Hajime Kotoura, Masaki Aota, Akira Miura, Satoru Suwa, Chuwa Tei, Ryuzo Sakata, Shuichi Hamasaki, Hiroyuki Yamamoto, Takeshi Aoyama, Takahiro Sakurai, Mitsuo Matsuda, Masahiko Onoe, Yuzo Takeuchi, Ryuji Nohara, Kimisato Nakano, Shigefumi Morioka, Yukikatsu Okada, Kenichi Shiratori, Yasuki Kihara, Michihiro Nasu, Masakiyo Nobuyoshi, Hitoshi Okabayashi, Hitoshi Yasumoto, Jyota Nakano, Tomoyuki Murakami, Katsuya Ishida, Hisao Ogawa, Michio Kawasuji, Seigo Sugiyama, Shoichiro Hagiwara, Kazuaki Mitsudo, Tatsuhiko Komiya, Kazushige Kadota, Masashi Komeda, Ryozo Tatami, Teruaki Ushijima, Akira Yoshida, Hiroyuki Nakajima, Shinji Miki, Ryuichi Hattori, Noboru Nishiwaki, Manabu Shirotani, Hiroshi Kato, Hiroshi Eizawa, Masaru Tanaka, Kazuaki Minami, Minoru Horie, Tohru Asai, Hiroyuki Takashima, Ryuji Higashita, Mamoru Takahashi, Takafumi Tahata, Yoshiki Matoba, Kiyosbi Doyama, Makoto Araki, Akinori Takizawa, Mitsuomi Shimamoto, Fumio Yamazaki, Osamu Doi, Hirofumi Kambara, Katsuhiko Matsuda, Satoshi Kaburagi, Masafumi Nara, Masaki Kawanami, Takashi Konishi, Yoshihisa Nakagawa
    Circulation Journal 73(8) 1459-1465 2009年08月
    Background: The prevalence of coronary artery disease (CAD) is increasing in young adults. Risk factor profiling will help to prevent heart attacks in young patients. This study aimed to analyze the risk factor profile and predictors of major cardiovascular events (MACE) in young CAD patients. Methods and Results: From the Coronary REvascularization Demonstrating Outcome study in the Kyoto (CREDO-Kyoto) registry of Japanese patients undergoing their first coronary revascularization, 6,320 patients with complete data for all variables for statistical analyses were divided into younger (≤55 years; n=898; 14.3%) and older ( > 55 years; n=5,422; 85.7%) patients. The risk factors that were more prevalent in the younger patients than in the older patients included: male sex, body mass index of > 25kg/m 2 , current smoker, family history of CAD, dyslipidemia and metabolic syndrome-like risk factor accumulation. Multivariate analyses revealed that chronic kidney disease (CKD) was the only significant predictor of MACE, the composite of cardiovascular death, myocardial infarction and cerebrovascular accident, in the younger patients. Importance of CKD as a prognostic factor was consistently shown by a multivariate analysis in the older patients. Conclusions: Accumulation of multiple risk factors is prevalent and CKD is associated with MACE in young Japanese CAD patients.
  • 心臓交感神経指標としての(冠状静脈洞-大動脈幹)ノルエピネフリン濃度較差(4.バイオマーカー・遺伝子多型とリスク評価,<特集>第73回日本循環器学会学術集会)
    蔦本 尚慶, 西山 敬三, 山路 正之, 河原 千穂, 山本 孝, 藤井 応理, 堀江 稔
    循環器専門医 : 日本循環器学会専門医誌 17(2) 243-249 2009年09月
  • Effect of carvedilol on plasma adiponectin concentration in patients with chronic heart failure
    Masayuki Yamaji, Takayoshi Tsutamoto, Toshinari Tanaka, Chiho Kawahara, Keizo Nishiyama, Takashi Yamamoto, Masanori Fujii, Minoru Horie
    Circulation Journal 73(6) 1067-1073 2009年06月
    Background: Patients with a high plasma adiponectin have a poor prognosis in chronic heart failure (CHF). Angiotensin-Converting enzyme inhibitors and angiotensin II receptor blockers are reported to increase the plasma adiponectin concentration, but the effect of β-blockers on plasma adiponectin in patients with CHF remains unknown. Methods and Results: Blood samples were collected at before and 6 months after administration of carvedilol in 44 CHF patients. The hemodynamic parameters, echocardiography, plasma concentrations of brain natriuretic peptide (BNP), norepinephrine and adiponectin were measured. Six months after treatment, there were significantly decreased plasma concentrations of adiponectin (15.8±1.4 to 11.0±1.1μg/ml, P < 0.0001), BNP and norepinephrine and increased left ventricular ejection fraction (LVEF). On stepwise multivariable analyses, a higher plasma adiponectin concentration before treatment (rs=-0.561, P < 0.0001) was a significant independent predictor of a greater decrease in adiponectin concentration and the decrease in plasma adiponectin concentration was significantly correlated with the improvement of LVEF (r=-0.561, P < 0.0001). Conclusions: These findings indicate that carvedilol decreases plasma adiponectin concentration and that the decrease in plasma adiponectin is associated with the improvement of LVEF after treatment with carvedilol in CHF patients.
  • Novel KCNE3 mutation reduces repolarizing potassium current and associated with long QT syndrome
    Seiko Ohno, Futoshi Toyoda, Dimitar P. Zankov, Dimitar P. Zankov, Hidetada Yoshida, Takeru Makiyama, Keiko Tsuji, Toshihiro Honda, Kazuhiko Obayashi, Hisao Ueyama, Wataru Shimizu, Yoshihiro Miyamoto, Shiro Kamakura, Hiroshi Matsuura, Toru Kita, Minoru Horie, Minoru Horie
    Human Mutation 30(4) 557-563 2009年04月
    Long QT syndrome(LQTS) is an inherited disease involving mutations in the genes encoding a number of cardiac ion channels and a membrane adaptor protein. Among the genes that are responsible for LQTS, KCNE1 and KCNE2 are members of the KCNE family of genes, and function as ancillary subunits of Kv channels. The third KCNE gene, KCNE3, is expressed in cardiac myocytes and interacts with KCNQ1 to change the channel properties. However, KCNE3 has never been linked to LQTS. To investigate the association between KCNE3 and LQTS, we conducted a genetic screening of KCNE3 mutations and single nucleotide polymorphisms(SNPs) in 485 Japanese LQTS probands using DHPLC- WAVE system and direct sequencing. Consequently, we identified two KCNE3 missense mutations, located in the N- and C-terminal domains. The functional effects of these mutations were examined by heterologous expression systems using CHO cells stably expressing KCNQ1. One mutation, p.R99γH was identified in a 76-year-old woman who suffered torsades de pointes(TdP) after administration of disopyramide. Another mutation, p.T4A was identified in a 16-year-old boy and 67-year-old woman. Although the boy carried another KCNH2 mutation, he was asymptomatic. On the other hand, the woman suffered from hypokalemia-induced TdP. In a series of electrophysiological analyses, the KCNQ1(Q1) +KCNE3(E3)-R99γH channel significantly reduced outward current compared to Q1+E3-WT, though the current density of the Q11E3-T4A channel displayed no statistical significance. This is the first report of KCNE3 mutations associated with LQTS. Screening for variants in the KCNE3 gene is of clinical importance for LQTS patients. © 2009 Wiley-Liss,Inc.
  • 心不全マーカーと心血管リスク予測因子としてのナトリウム利尿ペプチド
    蔦本 尚慶, 堀江 稔
    臨床薬理 = Japanese journal of clinical pharmacology 40(4) 173-174 2009年07月
  • Evaluation of channel function after alteration of amino acid residues at the pore center of KCNQ1 channel
    Taruna Ikrar, Taruna Ikrar, Haruo Hanawa, Hiroshi Watanabe, Yoshiyasu Aizawa, Mahmoud M. Ramadan, Masaomi Chinushi, Minoru Horie, Yoshifusa Aizawa
    Biochemical and Biophysical Research Communications 378(3) 589-594 2009年01月
    The effect of the electrical charge or the size of the amino acid residue at the pore center of a slowly activation component of the delayed rectifier potassium channel: KCNQ1 was studied. K + currents were measured after transfection of one of four KCNQ1 mutants: substituting Isoleucine with Lysine, Glutamate, Valine or Glycine and then transfected in COS-7 cells. Both the negatively- and positive charged residue I313 K and I313E showed a loss of function when expressed alone and a dominant negative suppression when co-expressed with wild type KCNQ1. When the site was substituted with the smallest neutral amino acid residue: I313G, there was a small reduction of current when transfected alone and a gain of function when co-transfected with the wild type. I313V showed no difference from the wild type. Changes of amino acid residue at the pore center of KCNQ1 may alter the channel function but this depends on the electrical charge or the size of amino acid residue. © 2008 Elsevier Inc. All rights reserved.
  • Inhibitory actions of the phosphatidylinositol 3-kinase inhibitor LY294002 on the human Kv1.5 channelPAPER
    J. Wu, J. Wu, J. Wu, W. G. Ding, H. Matsuura, H. Matsuura, K. Tsuji, W. J. Zang, M. Horie
    British Journal of Pharmacology 156(2) 377-387 2009年01月
    Background and purpose: Kv1.5 channels conduct the ultra-rapid delayed rectifier potassium current (I Kur ), and in humans, Kv1.5 channels are highly expressed in cardiac atria but are scarce in ventricles. Pharmacological blockade of human Kv1.5 (hKv1.5) has been regarded as effective for prevention and treatment of re-entry-based atrial tachyarrhythmias. Here we examined blockade of hKv1.5 channels by LY294002, a well-known inhibitor of phosphatidylinositol 3-kinase (PI3K). Experimental approach: hKv1.5 channels were heterologously expressed in Chinese hamster ovary cells. Effects of LY294002 on wild-type and mutant (T462C, H463C, T480A, R487V, A501V, I502A, I508A, L510A and V516A) hKv1.5 channels were examined by using the whole-cell patch-clamp method. Key results: LY294002 rapidly and reversibly inhibited hKv1.5 current in a concentration-dependent manner (IC 50 of 7.9 ̄mol·L -1 ). In contrast, wortmannin, a structurally distinct inhibitor of PI3K, had little inhibitory effect on hKv1.5 current. LY294002 block of hKv1.5 current developed with time during depolarizing voltage-clamp steps, and this blockade was also voltage-dependent with a steep increase over the voltage range for channel openings. The apparent binding (k +1 ) and unbinding (k -1 ) rate constants were calculated to be 1.6 ̄mol·L -1-1 ·s -1 and 5.7 s -1 respectively. Inhibition by LY294002 was significantly reduced in several hKv1.5 mutant channels: T480A, R487V, I502A, I508A, L510A and V516A. Conclusions and implications: LY294002 acts directly on hKv1.5 currents as an open channel blocker, independently of its effects on PI3K activity. Amino acid residues located in the pore region (Thr480, Arg487) and the S6 segment (Ile502, Ile508, Leu510, Val516) appear to constitute potential binding sites for LY294002. Mandarin translation of abstract. © 2009 The British Pharmacological Society.
  • QT延長症候群 (特集 小児疾患における臨床遺伝学の進歩) -- (話題の疾患遺伝子)
    堀江 稔
    小児科 50(7) 1083-1087 2009年06月
  • アップストリーム治療 (特集 心房細動) -- (心房細動の治療)
    堀江 稔
    診断と治療 97(5) 1022-1027 2009年05月
  • 薬剤性QT延長症候群 (特集 危険な不整脈の予防と治療)
    堀江 稔
    ICUとCCU 33(1) 19-24 2009年01月
  • Cinnamyl-3,4-dihydroxy-α-cyanocinnamate and nordihydroguaiaretic acid inhibit human Kv1.5 currents independently of lipoxygenase
    Ying Zi Gong, Ying Zi Gong, Ying Zi Gong, Wei Guang Ding, Jie Wu, Keiko Tsuji, Minoru Horie, Hiroshi Matsuura
    European Journal of Pharmacology 600(1-3) 18-25 2008年12月
    In humans, Kv1.5 (hKv1.5) channels conduct the ultra-rapid delayed rectifier K + current (I Kur ) that is important for the repolarization of cardiac action potentials. We aimed at examining the effect of lipoxygenase inhibitors cinnamyl-3,4-dihydroxy-α-cyanocinnamate (CDC), nordihydroguaiaretic acid (NDGA), and gossypol on hKv1.5 wild-type and mutant channels heterologously expressed in Chinese hamster ovary (CHO) cells, by use of the site-directed mutagenesis and whole-cell patch-clamp method. CDC and NDGA, but not gossypol, a structurally dissimilar inhibitor, reversibly inhibited hKv1.5 current in a concentration-dependent manner with IC 50 of 5.7 μM and 16.4 μM, respectively. The blockade evoked by both drugs was voltage-dependent between - 20 and + 10 mV (voltage range of channel opening). Moreover, this blocking action was found to progress with time during depolarizing voltage steps with a more rapid block at higher concentrations. CDC induced slight but significant delay of the deactivation rate. However, NDGA markedly slowed the deactivation time course, resulting in a tail crossover phenomenon. The recovery time constants from current block at repolarizing potentials for CDC and NDGA were 60.9 ms and 129.7 ms, respectively. Mutation of arginine 487 to valine (R487V) in the outer pore region of the channel significantly reduced the CDC action. These results demonstrate for the first time that CDC and NDGA block hKv1.5 channels by binding to the open state of the channels, independently of their effects on lipoxygenase activity. The putative binding site for CDC appears to be related to arginine 487 located in the outer pore region. © 2008 Elsevier B.V. All rights reserved.
  • QT延長症候群
    小児科 50(7) 1083-1087 2009年
  • Better survival with statin administration after revascularization therapy in Japanese patients with coronary artery disease - Perspectives from the CREDO-Kyoto Registry
    Yutaka Furukawa, Yutaka Furukawa, Yutaka Furukawa, Ryoji Taniguchi, Natsuhiko Ehara, Neiko Ozasa, Yoshisumi Haruna, Naritatsu Saito, Takahiro Doi, Kozo Hoshino, Satoshi Shizuta, Takeshi Morimoto, Takeshi Morimoto, Yukiko Imai, Satoshi Teramukai, Satoshi Teramukai, Masanori Fukushima, Masanori Fukushima, Toru Kita, Takeshi Kimura, Takeshi Kimura, Jong Dae Lee, Kuniyoshi Tanaka, Katsuo Okazaki, Masaaki Takahashi, Teiji Oda, Shigeo Matsui, Naohiro Ohashi, Eiichi Matsuyama, Makoto Kadoya, Yoshiki Takatsu, Shinichi Nomoto, Kazuaki Kataoka, Hajime Kotoura, Masaki Aota, Akira Miura, Satoru Suwa, Chuwa Tei, Ryuzo Sakata, Shuichi Hamasaki, Hiroyuki Yamamoto, Takeshi Aoyama, Takahiro Sakurai, Mitsuo Matsuda, Masahiko Onoe, Yuzo Takeuchi, Ryuji Nohara, Kimisato Nakano, Shigefumi Morioka, Yukikatsu Okada, Kenichi Shiratori, Yasuki Kihara, Michihiro Nasu, Masakiyo Nobuyoshi, Hitoshi Okabayashi, Hitoshi Yasumoto, Jyota Nakano, Tomoyuki Murakami, Katsuya Ishida, Hisao Ogawa, Michio Kawasuji, Seigo Sugiyama, Shoichiro Hagiwara, Kazuaki Mitsudo, Tatsuhiko Komiya, Kazushige Kadota, Masashi Komeda, Ryozo Tatami, Teruaki Ushijima, Akira Yoshida, Hiroyuki Nakajima, Shinji Miki, Ryuichi Hattori, Noboru Nishiwaki, Manabu Shirotani, Hiroshi Kato, Hiroshi Eizawa, Masaru Tanaka, Kazuaki Minami, Minoru Horie, Tohru Asai, Hiroyuki Takashima, Ryuji Higashita, Mamoru Takahashi, Takafumi Tahata, Yoshiki Matoba, Kiyoshi Doyama, Makoto Araki, Akinori Takizawa, Mitsuomi Shimamoto, Fumio Yamazaki, Osamu Doi, Hirofumi Kambara, Katsuhiko Matsuda, Satoshi Kaburagi, Masafumi Nara, Masaki Kawanami, Takashi Konishi, Kazunobu Nishimura, Seiji Ootani
    Circulation Journal 72(12) 1937-1945 2008年12月
    Background: The importance of statins in cardiovascular prevention has been demonstrated in various patient subsets. This study aimed to evaluate the effects of statins on long-term outcomes of Japanese patients undergoing their first coronary revascularization. Methods and Results: A total of 9,225 patients undergoing their first coronary revascularizations during 2000-2002 were divided into 2 groups according to the use of statins at discharge; patients with acute myocardial infarction were not included. Statins was administered to only 28.5% (n=2,630) of the patients. The median follow-up period was 3.5 years. Patients on statin therapy showed lower all-cause (5.2% vs 10.0%; p < 0.0001) and cardiovascular (3.2% vs 6.2%; p < 0.0001) mortality than those without statins (n=6,595) by Kaplan-Meier analysis and log-rank test. After adjustment by multivariate analysis according to 29 variables, statin therapy remained as an independent predictor of reduced all-cause (relative risk ratio (RR) 0.71, 95% confidence interval (CI) 0.59-0.86, p=0.0005) and cardiovascular (RR 0.72, 95% CI 0.56-0.91, p=0.0067) mortality. The validity of RR of statin therapy in multivariate analysis was further confirmed by risk adjustment using propensity scores (all-cause mortality: propensity-adjusted RR 0.70, 95% CI 0.58-0.85, p=0.0003; cardiovascular mortality: propensity-adjusted RR 0.70, 95% CI 0.54-0.89, p=0.0038). Conclusions: Statin therapy started at hospital discharge was associated with increased chance of survival in Japanese patients undergoing their first coronary revascularization.
  • Transcardiac increase in norepinephrine and prognosis in patients with chronic heart failure
    Takayoshi Tsutamoto, Keizo Nishiyama, Hiroshi Sakai, Toshinari Tanaka, Masanori Fujii, Takashi Yamamoto, Masayuki Yamaji, Minoru Horie
    European Journal of Heart Failure 14(7 Supplement 1) 157-1214 2008年12月
    Background: No previous study has compared the transcardiac gradient of norepinephrine (NE) and the prognosis of patients with chronic heart failure (CHF). Aim: To evaluate the prognostic role of the transcardiac gradient of NE in patients with CHF. Methods: We measured haemodynamic parameters and plasma levels of NE, brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) in the aortic root (AO) and coronary sinus (CS) in 356 consecutive patients with CHF. Results: During a median follow-up of 3.5 years, 40 patients died. Transcardiac gradients of BNP (273 ± 276 vs. 472 ± 433 pg/mL, p < 0.0001), NT-proBNP (417 ± 700 vs. 928 ± 1093 pg/mL, p < 0.0001) and NE (114 ± 160 vs. 473 ± 992 pg/mL, p < 0.0001) were significantly higher in non-survivors than survivors. After adjustment for clinical variables associated with CHF including haemodynamics and neurohumoral factors, the transcardiac gradient of NE (p < 0.0001) and plasma log NT-proBNP (p < 0.0001) were independent prognostic predictors. Among 67 patients in whom 123 I-metaiodobenzylguanidine (MIBG) could be performed, transcardiac increase in NE was correlated with the washout rate (r = 0.398, p = 0.0009) and was a superior predictor of mortality than MIBG parameters on stepwise multivariable Cox proportional hazards regression analyses. Conclusion: The transcardiac increase in NE is an independent and useful prognostic predictor for evaluating the prognosis of CHF patients. © 2008 European Society of Cardiology.
  • 第13回 : 日本心電学会学術奨励賞
    堀江 稔
    心電図 = Electrocardiology 28(6) 2008年12月
  • Constrictive pericarditis as an emerging manifestation of hyper-IgG4 disease
    Toshiro Sugimoto, Yoshikata Morita, Keiji Isshiki, Takashi Yamamoto, Takashi Uzu, Atsunori Kashiwagi, Minoru Horie, Tohru Asai
    International Journal of Cardiology 130(3) 100-101 2008年11月
    A 68-year-old Japanese man was admitted for evaluation of right pleural effusion and bilateral leg edema that had progressively worsened over 6 months. As chest computed tomography revealed marked pericardial thickening, we performed a pericardiectomy, resulting in the remarkable improvement of his clinical manifestations. However, pleural fibrosis associated with fever of unknown origin soon developed. An elevated serum level of serum IgG4 and infiltration of IgG4-positive plasma cell in the resected pericardium were identified; thus, our patient might have hyper-IgG4 disease. Our case is the first report describing constrictive pericarditis as an initial manifestation of hyper-IgG4 disease. © 2007 Elsevier Ireland Ltd. All rights reserved.
  • The factors contributing to whether or not hypertensive patients bring their home blood pressure record to the outpatient clinic
    Shinji Tamaki, Yasuyuki Nakamura, Masanori Teramura, Hiroshi Sakai, Tomoyuki Takayama, Tabito Okabayashi, Takeshi Kawashima, Minoru Horie
    Internal Medicine 47(18) 1561-1565 2008年11月
    Objective. We investigated the factors contributing to whether or not hypertensive patients brought their home blood pressure records to the outpatient clinic. Method. We studied 325 hypertensive patients [169 men (66.3±11.4 years old) and 156 women (68.1±11.2 years old)] who had received medical treatment for hypertension in our outpatient clinic from June to August 2006. Results. Of the 325 patients studied, 206 (63.4%, 101 men, 105 women) brought their home blood pressure records to our outpatient clinic. Logistic analysis showed age [odds ratio (OR) =0.95; 95% confidence interval (CI): 0.93-0.98; p=0.0002] , systolic blood pressure in outpatient clinic (OR=1.02; 95% CI: 1.00-1.04; p=0.0488) and the number of medicines prescribed (OR=1.94; 95% CI: 1.37-2.75; p=0.0002) were independent factors contributing to whether or not hypertensive patients bring along their home blood pressure records to the outpatient clinic. Conclusion. The contributing factors determining whether the patients bring their home blood pressure records to the outpatient clinic were: younger age, higher systolic blood pressure in the outpatient clinic, and a higher number of antihypertensive drugs. In conclusion, our results suggest that physicians should further motivate older patients, with well-controlled blood pressure in the outpatient clinic, to bring their home blood pressure records to the outpatient clinic. © 2008 The Japanese Society of Internal Medicine.
  • ペースメーカ、ICD、CRTを受けた患者の社会復帰・就学・就労に関するガイドライン
    奥村 謙, 安部 治彦, 小川 聡, 笠貫 宏, 鎌倉 史郎, 住友 直方, 新田 隆, 野島 俊雄, 堀江 正知, 松崎 益徳, 山口 巖, 江島 浩一郎, 金丸 浩, 菅野 重人, 佐々木 真吾, 豊島 健, 中島 博, 長友 敏寿, 野田 崇, 副島 京子, 村田 和也, 渡辺 重行, 大江 透, 加藤 貴雄, 田邉 晃久, 土肥 誠太郎, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 72 1133-1192 2008年11月
  • 血管炎症候群の診療ガイドライン
    尾崎 承一, 安藤 太三, 居石 克夫, 磯部 光章, 太田 敬, 小林 茂人, 重松 宏, 種本 和雄, 中島 康雄, 中林 公正, 能勢 眞人, 松永 尚文, 宮田 哲郎, 由谷 親夫, 吉田 雅治, 吉田 晃敏, 有村 義宏, 石津 明洋, 岩井 武尚, 岡崎 貴裕, 岡田 宗正, 片岡 浩, 金子 一成, 川名 誠司, 木田 一成, 小林 泰之, 古森 公浩, 坂本 一郎, 椎谷 紀彦, 重松 邦広, 高橋 淳士, 滝澤 始, 長岡 泰司, 長澤 浩平, 野島 美久, 橋本 博史, 濱口 真吾, 廣村 桂樹, 深谷 修作, 正木 久男, 松本 常男, 山田 秀裕, 吉田 俊治, 熊谷 俊一, 小池 隆夫, 笹嶋 唯博, 福井 次矢, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 72 1253-1346 2008年11月
  • ペースメーカ、ICD、CRTを受けた患者の社会復帰・就学・就労に関するガイドライン(循環器病の診断と治療に関するガイドライン(2006-2007年度合同研究班報告))
    奥村 謙, 安部 治彦, 小川 聡, 笠貫 宏, 鎌倉 史郎, 住友 直方, 新田 隆, 野島 俊雄, 堀江 正知, 松崎 益徳, 山口 巖, 江島 浩一郎, 金丸 浩, 菅野 重人, 佐々木 真吾, 豊島 健, 中島 博, 長友 敏寿, 野田 崇, 副島 京子, 村田 和也, 渡辺 重行, 大江 透, 加藤 貴雄, 田邉 晃久, 土肥 誠太郎, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 72(0) 1133-1174 2008年11月
  • ペースメーカ、ICD、CRTを受けた患者の社会復帰・就学・就労に関するガイドライン(ダイジェスト版,循環器病の診断と治療に関するガイドライン(2006-2007年度合同研究班報告))
    奥村 謙, 安部 治彦, 小川 聡, 笠貫 宏, 鎌倉 史郎, 住友 直方, 新田 隆, 野島 俊雄, 堀江 正知, 松崎 益徳, 山口 巖, 江島 浩一郎, 金丸 浩, 菅野 重人, 佐々木 真吾, 豊島 健, 中島 博, 長友 敏寿, 野田 崇, 副島 京子, 村田 和也, 渡辺 重行, 大江 透, 加藤 貴雄, 田邉 晃久, 土肥 誠太郎, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 72(0) 1175-1192 2008年11月
  • 血管炎症候群の診療ガイドライン(循環器病の診断と治療に関するガイドライン(2006-2007年度合同研究班報告))
    尾崎 承一, 安藤 太三, 居石 克夫, 磯部 光章, 太田 敬, 小林 茂人, 重松 宏, 種本 和雄, 中島 康雄, 中林 公正, 能勢 眞人, 松永 尚文, 宮田 哲郎, 由谷 親夫, 吉田 雅治, 吉田 晃敏, 有村 義宏, 石津 明洋, 岩井 武尚, 岡崎 貴裕, 岡田 宗正, 片岡 浩, 金子 一成, 川名 誠司, 木田 一成, 小林 泰之, 古森 公浩, 坂本 一郎, 椎谷 紀彦, 重松 邦広, 高橋 淳士, 滝澤 始, 長岡 泰司, 長澤 浩平, 野島 美久, 橋本 博史, 濱口 真吾, 廣村 桂樹, 深谷 修作, 正木 久男, 松本 常男, 山田 秀裕, 吉田 俊治, 熊谷 俊一, 小池 隆夫, 笹嶋 唯博, 福井 次矢, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 72(0) 1253-1318 2008年11月
  • 血管炎症候群の診療ガイドライン(ダイジェスト版,循環器病の診断と治療に関するガイドライン(2006-2007年度合同研究班報告))
    尾崎 承一, 安藤 太三, 居石 克夫, 磯部 光章, 太田 敬, 小林 茂人, 重松 宏, 種本 和雄, 中島 康雄, 中林 公正, 能勢 眞人, 松永 尚文, 宮田 哲郎, 由谷 親夫, 吉田 雅治, 吉田 晃敏, 有村 義宏, 石津 明洋, 岩井 武尚, 岡崎 貴裕, 岡田 宗正, 片岡 浩, 金子 一成, 川名 誠司, 木田 一成, 小林 泰之, 古森 公浩, 坂本 一郎, 椎谷 紀彦, 重松 邦広, 高橋 淳士, 滝澤 始, 長岡 泰司, 長澤 浩平, 野島 美久, 橋本 博史, 濱口 真吾, 廣村 桂樹, 深谷 修作, 正木 久男, 松本 常男, 山田 秀裕, 吉田 俊治, 熊谷 俊一, 小池 隆夫, 笹嶋 唯博, 福井 次矢, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 72(0) 1319-1346 2008年11月
  • 虚血性心疾患 虚血性心疾患の概念と病態生理 (新時代の糖尿病学(4)病因・診断・治療研究の進歩) -- (糖尿病に起因する合併症 慢性合併症--大血管症)
    堀江 稔
    日本臨床 66(0) 349-353 2008年11月
  • 68) QT延長症候群として経過観察中に心肺停止となった一例(第105回日本循環器学会近畿地方会)
    城日 加里, 福山 恵, 八尾 武憲, 中澤 優子, 伊藤 英樹, 芦原 貴司, 杉本 喜久, 伊藤 誠, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 72(0) 2008年10月
  • Cardiac scintigraphic findings of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes: A case report
    Shinro Matsuo, Kenichi Nakajima, Seigo Knuya, Yuichi Sato, Naoya Matsumoto, Minoru Horie
    Experimental and Clinical Cardiology 13 93-95 2008年06月
    A 49-year-old woman was admitted to hospital because of heart failure. She was diagnosed as having mitochondrial cardiomyopathy and diabetes mellitus. Echocardiography revealed a hypertrophic and poorly contracting left ventricle. A diagnosis of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes was established by muscle biopsy. She underwent technetium-99m-sestamibi ( 99m Tc-MIBI) and beta-methyl-p- 123 I-iodophenyl-pentadecanoic acid ( 123 I-BMIPP) scintigraphic examinations. 99m Tc-MIBI single-photon emission computed tomography revealed reduced tracer uptake in the hypertrophic left ventricular inferior wall. In contrast, there was an increase in 123I -BMIPP uptake in the in the region of reduced 99m Tc-MIBI uptake ( 99m Tc-MIBI/ 123 I-BMIPP mismatch). There was rapid washout of 99m Tc-MIBI from the myocardium (washout rate increased by 30%). Decreased 99m Tc-MIBI and increased 123 I-BMIPP uptake ( 99m Tc-MIBI/ 123 I-BMIPP mismatch) were the characteristics of cardiac involvement in mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. © 2008 Pulsus Group Inc. All rights reserved.
  • 145) 早期血栓閉塞型大動脈解離により心肺停止に至ったと考えられた一症例(第105回日本循環器学会近畿地方会)
    太田 宗樹, 藤井 応理, 堀江 稔, 藤野 和典, 浜本 徹, 佐々木 禎治, 五月女 隆男, 江口 豊
    Circulation journal : official journal of the Japanese Circulation Society 72(0) 2008年10月
  • Beneficial effect of perindopril on cardiac sympathetic nerve activity and brain natriuretic peptide in patients with chronic heart failure - Comparison with enalapril
    Takayoshi Tsutamoto, Takayoshi Tsutamoto, Toshinari Tanaka, Hiroshi Sakai, Keizo Nishiyama, Masanori Fujii, Takashi Yamamoto, Ichiro Nakae, Masato Ohnishi, Atsuyuki Wada, Minoru Horie
    Circulation Journal 72(5) 740-746 2008年05月
    Background: In patients with chronic heart failure (CHF), it remains unclear whether perindopril is more cardioprotective than enalapril. Methods and Results: Forty-five stable CHF outpatients undergoing conventional therapy including enalapril therapy were randomized to 2 groups [group I (n=24): continuous enalapril treatment; group II (n=21): enalapril was changed to perindopril]. Cardiac sympathetic nerve activity was evaluated using cardiac 123 I-metaiodobenzylguanidine (MIBG) scintigraphy, hemodynamic parameters and neurohumoral factors before and 6 months after treatment. There was no difference in baseline characteristics between the 2 groups. In group I, there were no changes in MIBG parameters, left ventricular ejection fraction (LVEF) or plasma level of brain natriuretic peptide (BNP). In contrast, in group II the delayed heart/mediastinum count ratio was significantly increased (2.0±0.07 vs 2.15±0.07, p=0.013) and the washout rate was significantly decreased (33.0±1.4 vs 30.5±1.2, p=0.030) after 6 months com pared with the baseline value. In addition, LVEF was significantly increased and the plasma BNP level was significantly decreased. Conclusion: These findings suggest that for the treatment of CHF, perindopril is superior to enalapril with respect of cardiac sympathetic nerve activity and BNP.
  • 心房細動は遺伝するのか? (特集 生活習慣病は遺伝するか?--家族性生活習慣病?)
    堀江 稔
    成人病と生活習慣病 38(10) 1180-1182 2008年10月
  • Mutation site dependent variability of cardiac events in Japanese LQT2 form of congenital long-QT syndrome
    Iori Nagaoka, Wataru Shimizu, Hideki Itoh, Satoshi Yamamoto, Tomoko Sakaguchi, Yuko Oka, Keiko Tsuji, Takashi Ashihara, Makoto Ito, Hidetada Yoshida, Seiko Ohno, Takeru Makiyama, Yoshihiro Miyamoto, Takashi Noda, Shiro Kamakura, Masaharu Akao, Minoru Horie, Minoru Horie
    Circulation Journal 72(5) 694-699 2008年05月
    Background: In the LQT2 form of long QT syndrome (LQTS), mutation sites are reported to correlate with clinical phenotypes in Caucasians, but the relationship in Asian patients remains unknown. The present study was designed to determine whether the location of KCNH2 mutations would influence the arrhythmic risk in LQT2 patients. Methods and Results: In 118 genetically-confirmed LQT2 patients (69 families, 62 KCNH2 mutations), the ECG parameters, Schwartz scores, and the incidence of cardiac events, defined as syncope, aborted cardiac arrest, and sudden cardiac death, were evaluated. To examine the effect of mutation sites, the participants were divided accordingly: pore (n=56) and non-pore (n=62) groups. The corrected QTend interval was significantly greater in the pore than in the non-pore group (QTc; 522±63ms vs 490±49 ms, p=0.002). In this study, the clinical course of each of the probands did not differ according to the mutation sites, whereas non-probands carrying the pore site mutation experienced their first cardiac events at significantly younger age than those with the non-pore site mutation (log-rank, p=0.0005). Conclusions: In a Japanese LQT2 cohort, family members with the pore site mutation were at higher arrhythmic risk than those with the non-pore site mutation.
  • 薬剤性QT延長症候群の遺伝子異常と分子病態(2.QT延長のサイエンス,<特集>第72回日本循環器学会学術集会)
    伊藤 英樹, 岡 優子, 堀江 稔
    循環器専門医 : 日本循環器学会専門医誌 16(2) 227-230 2008年09月
  • Effects of a 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitor, Fluvastatin, on Coronary Spasm After Withdrawal of Calcium-Channel Blockers
    Hirofumi Yasue, Yuji Mizuno, Eisaku Harada, Teruhiko Itoh, Hitoshi Nakagawa, Masafumi Nakayama, Hisao Ogawa, Shinji Tayama, Takasi Honda, Seiji Hokimoto, Shuichi Ohshima, Youichi Hokamura, Kiyotaka Kugiyama, Minoru Horie, Michihiro Yoshimura, Masaki Harada, Shiroh Uemura, Yoshihiko Saito
    Journal of the American College of Cardiology 51(18) 1742-1748 2008年05月
    Objectives: The purpose of this study was to determine whether a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) suppresses coronary spasm. Background: Coronary spasm is associated with endothelial dysfunction. Statins have been shown to improve endothelial function. Methods: This was a prospective, randomized, open-label, end point study. Sixty-four patients wh o had no significant organic coronary stenosis and in whom coronary spasm was induced by intracoronary injection of acetylcholine (ACh) were randomly assigned to fluvastatin 30 mg/day plus the conventional calcium-channel blocker (CCB) therapy (31 patients, statin group) or the conventional CCB therapy (33 patients, nonstatin group). After 6 months of treatment, the intracoronary injection of ACh was repeated and the coronary spasm was assessed. Results: Coronary spasm was suppressed in 16 of the 31 patients (51.5%, p < 0.0001) of the statin group and in 7 of the 33 patients (21.2%, p = 0.0110) of the nonstatin group after 6 months of treatment. Thus, the number of patients with ACh-induced coronary spasm was significantly reduced in the statin group as compared with the nonstatin group (51.6% vs. 21.2%, p = 0.0231) after 6 months of treatment. Conclusions: The addition of fluvastatin 30 mg/day to the conventional CCB therapy for 6 months significantly reduced the number of patients with ACh-induced coronary spasm as compared with the conventional CCB therapy. Thus, a statin (fluvastatin) may possibly be a novel therapeutic drug for coronary spasm. © 2008 American College of Cardiology Foundation.
  • 循環器疾患の遺伝子学 (臨床遺伝子学'08)
    堀江 稔
    最新医学 63(0) 1814-1826 2008年09月
  • Whole-body periodic acceleration enhances brachial endothelial function
    Tetsuya Matsumoto, Tetsuya Matsumoto, Masatoshi Fujita, Yasuhiro Tarutani, Tetsunobu Yamane, Hiroyuki Takashima, Ichiro Nakae, Minoru Horie
    Circulation Journal 72(1) 139-143 2008年03月
    Background: Periodic acceleration in the direction of the spinal axis through repetitive movement increases the shear stress on the vascular endothelium. In the present study it was assessed whether whole-body periodic acceleration with a new device would enhance endothelial function in sedentary adult volunteers. Methods and Results: Twenty-six sedentary subjects (44±3 years) were randomly assigned to remain sedentary or perform exercise training for 4 weeks, followed by crossover. Periodic acceleration was applied with a horizontal motion platform at 2-3 Hz and approximately ±2.2 m/s 2 for 45 min. Increases in the brachial artery diameter were examined at rest, during reactive hyperemia (flow-mediated dilatation: %FMD) and after sublingual administration of 0.3 mg nitroglycerin (%NTG) using high-resolution ultrasound. All subjects completed the study with no adverse side-effects. There were no significant changes in the resting heart rate or arterial pressure, body weight, or lipid profiles during the study. Although %FMD did not change during the non-training period with periodic acceleration, it significantly increased from 7.3±0.4% at baseline to 8.4±0.4% after the training period (p < 0.05), while %NTG remained unchanged. Conclusions: Whole-body periodic acceleration with a horizontal motion platform improved vascular endothelial function in sedentary adults. This device might offer an alternative to active exercise for patients whose medical condition limits physical activity.
  • 69) 早期の心臓再同期療法が有効であったLamin A/C遺伝子関連心筋症の1家系(第104回日本循環器学会近畿地方会)
    牧山 武, 赤尾 昌治, 静田 聡, 土井 孝浩, 大野 聖子, 西尾 由貴子, 西山 慶, 木村 剛, 北 徹, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 72(0) 2008年04月
  • 112) 縦隔手術および縦隔放射線治療後に右心不全が慢性化し,特異な右心圧波形を示した一例(第104回日本循環器学会近畿地方会)
    羽野 嘉文, 山根 哲信, 蔦本 尚慶, 藤井 応理, 高島 弘行, 山本 孝, 松本 祐一, 北川 直孝, 中江 一郎, 伊藤 誠, 堀江 稔, 東 秋弘
    Circulation journal : official journal of the Japanese Circulation Society 72(0) 2008年04月
  • 137) 閉塞性肥大型心筋症に対し経皮的中隔心筋焼灼術を施行した一例(第104回日本循環器学会近畿地方会)
    角野 元彦, 羽野 嘉文, 北川 直孝, 松本 祐一, 八尾 武憲, 山根 哲信, 城 日加里, 山本 孝, 高島 弘行, 藤井 応理, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 72(0) 2008年04月
  • 150) PKP2遺伝子変異が同定された不整脈源性右室心筋症(ARVC)の1剖検例(第104回日本循環器学会近畿地方会)
    松本 祐一, 長岡 伊織, 伊藤 誠, 堀江 稔, 西尾 由貴子, 杉原 洋行, 川嶋 剛史
    Circulation journal : official journal of the Japanese Circulation Society 72(0) 2008年04月
  • 第16回 体表心臓微小電位研究会 シンポジウム T波解析と不整脈原生: From simulation practice Microvolt T wave alternansが反映する心室性不整脈発生基質:コンピュータシミュレーションによる基礎的検討
    芦原 貴司, 八尾 武憲, 伊藤 誠, 堀江 稔, 難波 経豊, 原口 亮, 中沢 一雄, 池田 隆徳
    心臓 39(1) 14-19 2007年
    巨視的なT wave alternans(TWA)は致死性の心室性不整脈の予兆として知られる.一方で,最近,微視的なmicrovolt T wave altemans(MTWA)が心臓突然死につながる心室性不整脈の非侵襲的予知指標として注目されるようになった.TWAの成因としては活動電位持続時間(APD)の回復曲線にもとつくalternansや,不均質性にもとづく興奮波の分裂や回り込みが考えられているが,MTWAの成因については明らかでない.本研究では,コンピュータシミュレーションによりTWAとMTWAを再現し,MTWAの成因とそれが反映する不整脈発生基質について検討した.ヒト心室筋活動電位モデルで1-2次元の正常心筋モデルと,種々のイオンチャネルやgap結合のパラメータを変化させた異常心筋モデルを構成し,計算で描いた心電図からTWAとMTWAを検出した.正常心筋モデルでTWAは再現されたが,MTWAは陽性基準を満たさなかった.異常心筋モデルではMTWAが陽性となる例が存在したが,異常の種類によって,APD回復曲線の急峻化を伴うもの,APD回復曲線の平坦化を伴うもの,興奮伝播異常を伴うものの3つに分類された.MTWA陽性例では,心電図上のみならず膜電位やCa transientの分布マップ上でも,変化が目視では認識できなかった.MTWAは心室性不整脈の発生基質となりうる心筋異常を反映するが,TWAとは種々の点で異なった性質を有しており,MTWAはTWAの延長線上にあるものではないことが推察される.
  • 第41回 理論心電図研究会 チャネル病の修飾因子:総論
    伊藤 英樹, 牧山 武, 辻 啓子, 坂口 知子, 長岡 伊織, 岡 優子, 芦原 貴司, 伊藤 誠, 大野 聖子, 赤尾 昌治, 堀江 稔
    心臓 39(6) 576-579 2007年
    イオンチャネルは細胞膜に存在しイオンの細胞内外への移動を調節する蛋白で,イオンチャネルの開閉は神経や筋肉の興奮などをひき起こし生体の活動に必須である.これらのイオンチャネルをコードする遺伝子に変異が生じるとチャネルの開閉動態が変化し,適切なイオンの移動が障害されさまざまな疾患が発症する.イオンチャネルの遺伝子変異が原因となる疾患群は臓器が異なれども臨床面あるいは機能薬理的な側面で類似点が多く,"チャネル病"という概念で理解されている.とくに心筋に存在するイオンチャネルの遺伝子異常はQT延長症候群やBrugada症候群などさまざまな不整脈の原因となるが,同じ遺伝子異常を認める症例においても臨床上その表現型,重症度はさまざまである.性別,年齢,変異の数,自律神経活動など多くの因子がこれらの臨床病態に修飾し,臨床病態を複雑にしていると考えられる.
  • イオンチャネル異常による致死性不整脈  心房筋細胞におけるAT1受容体を介した緩徐活性型遅延整流性K`+´電流(IKs)の増大と活動電位の短縮―心房細動治療におけるAT1受容体遮断薬の有効性との関連―
    松浦 博, Zankov Dimitar P., 尾松 万里子, 礒野 高敬, 豊田 太, 丁 維光, 堀江 稔
    心電図 27(2) 145-153 2007年
    緩徐活性型遅延整流性K+電流 (lKS) は活動電位プラトー相で活性化され活動電位持続時間 (APD) を決定する電流系の一つであり, ヒトを含む多くのほ乳類の心房筋や心室筋に存在することが知られている.AT1受容体遮断薬は心房細動の発生に対して抑制効果があることが報告されているが, その電気生理学的機序は十分には明らかにされていない.本研究の目的は, 心房筋細胞においてアンジオテンシンII (Ang II) によるlKsの修飾を検討し, 加えてそのAPDに及ぼす効果を明らかにすることとした, モルモット心房筋細胞に全細胞型パッチクランプ法を適用してlKs (voltage-clamp) ならびに活動電位 (current-clamp) を記録した.Ang IIならびにその安定化誘導体であるSar1-Ang IIはAT1受容体-Gタンパク質-ボスホリパーゼC-プロテインキナーゼC系を活性化してlKsを増大させ, それに伴いAPDを短縮させることが明らかとなった.本実験結果をヒト心房筋に外挿して考えると, AT1受容体遮断薬はAng IIによるlKs増大を介したAPD (ならびに有効不応期) の短縮作用に対して拮抗的にはたらくことが予想され, これがAT1受容体遮断薬のもつ心房細動に対する抑制効果の背景となる電気生理学的機序の一つであると考えられた.
  • HEART's Original [臨床研究] 全身の周期的加速運動の血管内皮機能に対する効果
    松本 鉄也, 藤田 正俊, 樽谷 康弘, 山根 哲信, 高島 弘行, 中江 一郎, 堀江 稔
    心臓 39(11) 986-991 2007年
    背景,目的:習慣的な運動は血管内皮機能を改善させ,心血管病のリスクを減少させる.その機序は血管内皮に作用するシェアストレスによると考えられている.そこで,臥床した状態で全身を上下に周期的に振動させる運動負荷ベッドを用いて,全身の周期的加速運動の血管内皮機能の改善効果について上腕動脈の反応性充血反応(FMD)を評価して検討した.
    方法:運動習慣のない成人ボランティア20名(平均年齢43±4歳,女性12名,男性8名)を対象とした.対象者を無作為に2群に分け,4週間の運動療法期間,4週間の非運動療法期間の順番をクロスオーバーにて割りつけた.1日1回,45分間の2~3Hz,±0.22gの運動を4週間の間に計20回施行した.
    結果:すべての対象者において運動装置による合併症は生じなかった.運動療法期間,非運動療法期間の前後で血圧,脈拍,脂質,血糖,Body Mass Index(BMI)に変化は認めなかった.運動療法群でFMDは73±0.6%から8.2±0.7%に有意に増加した(P<0.05).非運動療法群ではFMDに変化は認めなかった(7.2±0.6%から7.7±0.5%).硝酸薬による血管拡張作用は運動療法期間,非運動療法期間の前後で同様であった.
    結論:運動習慣のない成人において,全身の受動的な周期的加速運動は血管内皮機能を改善した.QOL向上・生命予後改善効果も含めた運動療法として期待される.
  • 第40回理論心電図研究会 熱変性高速液体クロマトグラフィ法を用いたリアノジン受容体遺伝子変異のスクリーニング
    松井 圭司, 長岡 伊織, 堀江 稔
    心臓 38(5) 533-535 2006年
    リアノジン受容体は,心筋収縮時の筋小胞体からのカルシウム放出をつかさどるイオンチャンネルである.近年,運動誘発性心室頻拍の患者において, リアノジン受容体の変異が報告されている. リアノジン受容体遺伝子は, 1 0 5個のエクソンを持つ比較的大きな構造を持っている.今まで報告されたリアノジン受容体変異の部位は,N末端近傍,中央部のFB結合蛋白部,C末端の筋小胞体膜貫通部の3カ所に集中している.
    われわれは,熱変性高速液体クロマトグラフィを用いて運動誘発性心室頻拍の患者のリアノジン受容体遺伝子変異をスクリーニングし,新規の変異を発見した.
  • 第3回不整脈薬物治療フォーラム 心筋Naチャネルの抗不整脈薬結合関連部位に遺伝子変異を認めたBrugada症候群の薬剤負荷試験と抗不整脈薬治療
    伊藤 英樹, 坂口 知子, 辻 啓子, 岡 優子, 中澤 優子, 八尾 武憲, 城 日加里, 長岡 伊織, 芦原 貴司, 伊藤 誠, 堀江 稔
    心臓 38(9) 979-980 2006年
    ピルジカイニドを投与してもST上昇を認めなかったBrugada症候群において見出された新変異(N406S)に対するIb群抗不整脈薬リドカインの薬理効果を,発現実験系で解析した.筆者らはこれまでに,N406S変異においては電位依存性活性が低下し,遅い不活性化を増強すること,およびピルジカイニドの薬剤感受性が著明に低下し,一方,キニジンの薬剤感受性がが亢進することを報告している.今回行ったリドカインによる検討では,リドカインによる使用依存性ブロックは著明に低下し,遅い不活性化からの回復は促進し電流抑制が軽減された.以上から,N406S変異を有するBrugada症候群の場合,Ib群抗不整脈薬による治療の可能性が示唆された.
  • Noninvasive identification of myocardial sympathetic and metabolic abnormalities in a patient with "Takotsubo" cardiomyopathy
    Shinro Matsuo, Tetsuya Matsumoto, Ichiro Nakae, Daisuke Masuda, Masahiko Takada, Kiyoshi Murata, Minoru Horie
    International Medical Journal 12 143-144 2005年06月
  • 家庭用心電計による不整脈の検出 : 非伝送携帯型心電計による検討
    伊藤 誠, 稲垣 菊代, 芦原 貴司, 中澤 優子, 城 日加里, 伊藤 英樹, 八尾 武憲, 杉本 喜久, 坂口 知子, 岡 優子, 堀江 稔, 桝野 みどり, 金光 陽子, 楠本 和也, 山本 則仁
    心電図 = Electrocardiology 28 "S-1-21"-"S-1-22" 2008年03月
  • 心房細動と遺伝子異常 (特集 変革する心房細動診療とその実践up-to-date)
    牧山 武, 赤尾 昌治, 堀江 稔
    内科 101(3) 517-521 2008年03月
  • 心不全のバイオマーカー--心腎相関 (第1土曜特集 心血管マルチバイオマーカー・ストラテジー) -- (心血管マルチバイオマーカー・ストラテジー)
    蔦本 尚慶, 堀江 稔
    医学のあゆみ 224(5) 318-325 2008年02月
  • 第21回犬山不整脈カンファランスメインテーマ不整脈の成因と治療戦略テーマI「不整脈の新しい分子メカニズム」:心臓イオンチャネル遺伝子の転写制御機構~エピジェネティックスと機能分化~
    鷹野 誠, 倉富 忍, 堀江 稔, 斉藤 能彦, 桑原 宏一郎
    心電図 27(3) 15-28 2007年
  • 第39回理論心電図研究会 Andersen症候群から学ぶU波の成因
    小堀 敦志, 堀江 稔
    心臓 37(6) 536-542 2005年
    Einthovenにより命名されたU波は,いまだにその成因や構造について明らかにされていない.また各種病態により生じる異常なU波についても不明なことが多く残されたままである.カリウムチャネルの遺伝子異常(KCNJ2)により骨格異常,周期性四肢麻痺,QT延長と心室性不整脈を来すAndersen症候群は,U波の異常を示す疾患として最近注目されている.われわれはこれまでに7家系13人のAndersen症候群患者から6つのKCNJ2遺伝子異常を同定した.計測可能であった12人のU波を検討したところ,平均振幅は0.23±0.02mVと増高,先行するT波との振幅比は0.95±0.2と異常高値であった.さらに心室性不整脈が80%の症例に認められ,その心室性期外収縮はR on U型となる長い連結期で出現していた.新たに同定された遺伝子異常(Gl46S)をパッチクランプ法により機能解析し,このデータを基に心筋活動電位モデル(Kyoto model)にてシミュレーションを行った.再分極の遅延により活動電位はなだらかに延長し,遅延後脱分極の発生につづく心室性期外収縮が観察された.これらのことによりAndersen症候群におけるU波の成因に,遅延後脱分極が関与している可能性が示唆された.
  • Additional Gene Variants Reduce Effectiveness of Beta-Blockers in the LQT1 Form of Long QT Syndrome
    Atsushi Kobori, Nobuaki Sarai, Wataru Shimizu, Yoshihide Nakamura, Yosuke Murakami, Takeru Makiyama, Seiko Ohno, Kotoe Takenaka, Tomonori Ninomiya, Yuichiro Fujiwara, Satoshi Matsuoka, Makoto Takano, Akinori Noma, Toru Kita, Minoru Horie, Minoru Horie
    Journal of Cardiovascular Electrophysiology 15(2) 190-199 2004年02月
    Introduction: Beta-blockers are widely used to prevent the lethal cardiac events associated with the long QT syndrome (LQTS), especially in KCNQ1-related LQTS (LQT1) patients. Some LQT1 patients, however, are refractory to this therapy. Methods and Results: Eighteen symptomatic LQTS patients (12 families) were genetically diagnosed as having heterozygous KCNQ1 variants and received beta-blocker therapy. Cardiac events recurred in 4 members (3 families) despite continued therapy during mean follow-up of 70 months. Three of these patients (2 families) had the same mutation [A341V (KCNQ1)]; and the other had R243H (KCNQ1). The latter patient took aprindine, which seemed to be responsible for the event. By functional assay using a heterologous mammalian expression system, we found that A341V (KCNQ1) is a loss-of-function type mutation (not dominant negative). Further genetic screening revealed that one A341V (KCNQ1) family cosegregated with S706C (KCNH2) and another with G144S (KCNJ2). Functional assay of the S706C (KCNH2) mutation was found to reduce the current density of expressed heterozygous KCNH2 channels with a positive shift (+8 mV) of the activation curve. Action potential simulation study was conducted based on the KYOTO model to estimate the influence of additional gene modifiers. In both models mimicking LQT1 plus 2 and LQT1 plus 7, the incidence of early afterdepolarization was increased compared with the LQT1 model under the setting of beta-adrenergic stimulation. Conclusion: Multiple mutations in different LQTS-related genes may modify clinical characteristics. Expanded gene survey may be required in LQT1 patients who are resistant to beta-blocker therapy.
  • 不整脈予防におけるARB, ACE阻害薬とアルドステロン拮抗薬 : アルドステロン拮抗薬と心室リモデリング
    蔦本 尚慶, 林 優, 田中 俊成, 西山 敬三, 山本 孝, 山路 正之, 藤井 応理, 伊藤 誠, 堀江 稔
    心電図 = Electrocardiology 28(1) 22-31 2008年01月
  • Bedside Teaching BNP測定における心不全患者の管理
    蔦本 尚慶, 堀江 稔
    呼吸と循環 52(2) 185-189 2004年02月
  • 採血でどこまでわかるか (心臓病のすべて) -- (心臓病を見つける)
    蔦本 尚慶, 堀江 稔
    からだの科学(257) 48-54 2008年
  • Thrombotic microangiopathy in an adult patient with clinically amyopathic dermatomyositis complicated with interstitial lung disease [2]
    Toshiro Sugimoto, Toshiro Sugimoto, T. Hajiro, T. Fujimoto, N. Kojyo, M. Horie, A. Kashiwagi
    Lupus 16(12) 1004-1005 2007年12月
  • 心不全のバイオマーカー ー心腎相関
    医学のあゆみ 224(5) 318-325 2008年
  • 第38回河口湖心臓討論会 「分子生物学から見た循環器疾患」イオンチャネルと循環器疾患
    堀江 稔
    心臓 37(1) 83-92 2005年
    ヒト・ゲノム・プロジェクトに先行して,興奮性細胞膜に多く発現するイオン・チャネル分子のクローニングやその機能解析は,種々の遺伝子導入法とパッチ・クランプの進歩に伴い急速に行われていたが,1990年代に入って,遺伝的に重症不整脈を起こす一群の病気が,詳細な遺伝解析の結果,判明した.最初に報告されたのは,家族性QT延長症候群の患者においてであり,心臓の興奮とその伝導に重要な働きをする心筋ナトリウム・チャネル(SCN5A)と再分極を調節する遅延整流カリウム・チャネル遺伝子(KCNH2)の種々な変異であった.その後,ヒトにおいて重要な,もう一つの遅延整流カリウム・チャネルをコードするKCNQ1遺伝子にも,異常が発見され,以前から連鎖解析法で調べられLQT1と呼ばれていたグループの原因遺伝子であることが判明した. このような研究がきっかけとなって,心筋イオン・チャネル病の研究は,この10年近くの間に急速に進んだ.
  • 心房筋リモデリングを考慮したヒト心房細動in silicoモデルにおけるアミオダロンの急性効果と慢性効果
    PROGRESS IN MEDICINE 28(1) 562-567 2008年
  • Syndrome X
    Tetsuya Matsumoto, Minoru Horie, Kenichi Mitsunami
    Nippon rinsho. Japanese journal of clinical medicine Suppl 5 Pt 2 143-146 2007年09月
  • BNP検査の総説 : NT-proBNP検査時代を迎えて
    蔦本 尚慶, 堀江 稔
    臨床病理 = THE OFFICIAL JOURNAL OF JAPANESE SOCIETY OF LABORATORY MEDICINE 55 2007年10月
  • Atrial fibrillation up to date. 4) Are prevention and modification of atrial remodeling possible?
    Minoru Horie
    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine 96 1909-1911 2007年09月
  • 107)右房内肉腫による上大静脈症候群に対しステント留置術を施行した一例(第103回日本循環器学会近畿地方会)
    藤井 応理, 河原 千穂, 高島 弘行, 松本 鉄也, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年10月
  • 74)新たなHERG遺伝子異常を認めた遺伝性QT延長症候群の一家系(第102回日本循環器学会九州地方会)
    安田 潮人, 加治 良一, 小田代 敬太, 中村 洋文, 辛島 詠士, 島津 秀樹, 深田 光敬, 中司 元, 丸山 徹, 宗内 淳, 堀江 稔, 辻 敬子
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年10月
  • 単一遺伝子病とゲノム(5)循環器疾患(2)不整脈
    堀江 稔
    ゲノム医学 7(3) 219-223 2007年10月
  • Romano-Ward syndrome
    Minoru Horie
    Nippon rinsho. Japanese journal of clinical medicine Suppl 4 230-233 2007年08月
  • Effect of angiotensin II receptor blockade on derived central arterial waveforms in hypertension
    Shinro Matsuo, Ichiro Nakae, Minoru Horie, Tetsuhiro Yamada, Yasuyuki Nakamura, Yasukazu Uchida, Yuichi Sato, Naoya Matsumoto
    Japanese Pharmacology and Therapeutics 35 801-807 2007年08月
    Objectives Arterial hypertension leads to vascular functional and structural adaptive processes which are related to angiotensin II. Analysis of the blood pressure (BP) waveform in the radial artery was introduced into clinical studies to characterize arterial properties by augmentation index (AI) or central blood pressure. The present study examined whether such properties were particularly responsive to angiotensin II receptor blocker therapy. Methods A total of 27 patients (63 ± 2.4 years) with essential hypertension [BP 152.8 ± 5.1/84.7 ± 4.0mmHg] were treated with olmesartan based on international guidelines. Radial artery pressure wave, including AI and BP2 (late systolic blood pressure), were determined by using an automatic cuff oscillometric device before and after therapy. Results Antihypertensive treatment with olmesartan [21.7 ± 1.7mg/day] significantly reduced brachial BP (152.8 ± 5.1 mmHg vs. 133.8 ± 3.3 mmHg, p = 0.0028) and BP2 (140.0 ± 5.1 mmHg vs. 120.3 ± 3.3 mmHg, p = 0.0006). AI decreased after 8 weeks of antihypertensive therapy (84.56 ± 2.58% vs. 76.85 ± 2.74%, p = 0.046). Plasma level of high sensitive C reactive protein was significantly decreased (0.462 ± 0.061 mg/dL vs. 0.202 ± 0.027 mg/dL, p = 0.003). Conclusions Olmesartan treatment reduces the AI as well as blood pressure in hypertensive patients.
  • Disorders of cardiac repolarization long QT and short QT syndromes
    Minoru Horie, Minoru Horie, Hideki Itoh
    Circulation Journal 71(SupplementA) 50-53 2007年07月
    The long and short QT syndromes are heterogeneous diseases characterized by abnormal ventricular repolarization and episodes of syncope and/or life-threatening cardiac arrhythmias. Several disease-causing genes have been identified, including those encoding cardiac ion channel-composing proteins. The clinical determination of genotype offers a striking benefit: diagnosis, prediction of clinical phenotype, risk stratification, clinical and genetic counseling, and introduction of therapy. Genetic testing is of special importance for the genotyped patient's family members to prevent unexpected cardiac death. By means of recently advanced methodology in molecular genetics and electrophysiology it is expected that novel genes responsible for these disease entities will be identified.
  • 心房細動 up to date : 4)心房リモデリングの予防と改善は可能か
    堀江 稔
    日本内科学会雑誌 96(9) 1909-1911 2007年09月
  • Protective mechanism of adenosine to the rat arterial endothelial dysfunction induced by hydrogen peroxide
    Jun Lu, Shu Ming Zhu, Wei Jin Zang, Wei Jin Zang, Xiao Li Xu, Hong Li Luo, Xiao Jiang Yu, Sheng Peng Wang, Shan Shan Kong, Jie Wu, Jie Wu, Minoru Horie, Lei Sun
    Biological and Pharmaceutical Bulletin 30(7) 1206-1211 2007年07月
    This study was designed to examine the in vitro effects of adenosine (Ado) on hydrogen peroxide-induced endothelial dysfunction in rats. Endothelial dysfunction was induced by exposing isolated rat mesenteric arteries to hydrogen peroxide (0.5 mM) for 12 h using an organ culture system. The protective effects of adenosine were tested by exposing isolated mesenteric arteries to adenosine (3 × 10 -7 mol/l, 10 -6 mol/l, 3 × 10 -6 mol/l) + hydrogen peroxide (0.5 mM) for 12 h. This exposure to hydrogen peroxide induced a significant concentration-dependent inhibition of endothelium-dependent relaxation (EDR). Coculture of segments of mesenteric artery with adenosine (3 × 10 -7 , 10 -6 , and 3 × 10 -6 mol/l) attenuated the hydrogen peroxide-induced impairment of vasorelaxation. This impairment was accompanied by a reduction in nitrite/nitrate, nitric oxide (NO) synthase (NOS), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and an increasing in malondislehyde (MDA) and lactate dehydrogenase (LDH) activities in the aorta. These results indicate that adenosine can be used to attenuate hydrogen peroxide-induced endothelial dysfunction, an effect that may be related to antioxidation, thus enhancing NO production by preventing the decrease in NOS. © 2007 Pharmaceutical Society of Japan.
  • 30-P3-1 調剤併設型ドラッグストアにおける携帯型心電計を用いた不整脈治療の病診連携への参加(地域連携・薬薬連携・その他,社会の期待に応える医療薬学を)
    奥村 朋子, 榊原 幹夫, 小栗 正寛, 島田 繁, 岡田 啓, 沢村 昭人, 荒井 恵二, 堀江 稔, 伊藤 誠, 芦原 貴司, 稲垣 菊代
    日本医療薬学会年会講演要旨集 17 2007年09月
  • QT延長症候群(先天性,後天性) (不整脈検査) -- (不整脈と疾病)
    坂口 知子, 堀江 稔
    臨床検査 51(7) 764-768 2007年07月
  • 1)ステントを留置せずに治療し得た抗リン脂質抗体症候群の若年発症急性心筋梗塞の一例(第102回日本循環器学会近畿地方会)
    松本 祐一, 楢谷 康弘, 吉野 知秀, 羽野 嘉文, 高山 智行, 環 愼二, 岡林 旅人, 川嶋 剛史, 山本 孝, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • 48)心房細動に対する拡大肺静脈隔離術後における携帯型心電計の有用性(第102回日本循環器学会近畿地方会)
    芦原 貴司, 中澤 優子, 八尾 武憲, 城 日加里, 伊藤 英樹, 八木 崇文, 杉本 喜久, 伊藤 誠, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • 49)不整脈源性右室心筋症に対してICD植え込み術を施行した一例(第102回日本循環器学会近畿地方会)
    四方田 真紀子, 松尾 信郎, 芦原 貴司, 八尾 武憲, 杉本 喜久, 松本 鉄也, 伊藤 誠, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • 52)前心室間静脈からのペーシング波形がVTと一致したが,大動脈弁左冠尖からの高周波通電により根治したsustained VTの一例(第102回日本循環器学会近畿地方会)
    國友 健生, 伊藤 英樹, 伊藤 誠, 八尾 武憲, 中澤 優子, 芦原 貴司, 城 日加里, 堀江 稔, 杉本 喜久
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • 59)心筋リアノジン受容体(hRYR2)の遺伝子変異を有したカテコラミン誘発性多形性心室頻拍(CPVT)の2症例(第102回日本循環器学会近畿地方会)
    道智 賢市, 松本 祐一, 長岡 伊織, 八尾 武憲, 坂口 知子, 中澤 優子, 岡 優子, 伊藤 英樹, 芦原 貴司, 伊藤 誠, 堀江 稔, 住友 直方, 鷹津 良樹
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • 117)糖尿病患者における冠動脈病変と冠動脈石灰化スコアの関連性の検討(第102回日本循環器学会近畿地方会)
    大村 寧, 近藤 基之, 本田 亘, 卯木 智, 西尾 善彦, 前川 聡, 柏木 厚典, 高島 弘行, 堀江 稔, 門脇 崇, 上島 弘嗣, 鈴木 英司, 吉村 達
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • The role of impaired sympathetic nerve function in enhancing coronary vasoconstriction in patients with hypertrophic cardiomyopathy
    Shinro Matsuo, Tetsuya Matsumoto, Ichiro Nakae, Minoru Horie
    Experimental and Clinical Cardiology 12 37-41 2007年04月
    Coronary vasospasm and diminished coronary blood flow reserve have often been reported in patients with hypertrophic cardiomyopathy (HCM). However, the mechanism of coronary spasm in HCM is unknown. Thus, coronary endothelial function and sympathetic nerve function in 11 patients with HCM and 11 control patients matched for age and sex were examined. The diameter of the left anterior descending coronary artery was assessed by quantitative coronary angiography, and the change in coronary blood flow was estimated using an intracoronary Doppler flow wire. To assess myocardial sympathetic nerve function, metaiodobenzylguanidine images - 15 min and 180 min after the injection of 1231-metaiodoben-zylguanidine at a dosage of 111 MBq - were obtained, and the heart to mediastinum (H/M) count ratio and the washout rate MR) were calculated. The H/M ratio was significantly lower in patients with HCM (2.1±0.3) than in control patients (2.6±0.4) (P < 0.01). In addition, the WR was higher in patients with HCM (35±6%) than in control patients (28±3%) (P < 0.01). The HCM subjects with coronary spasm had lower H/M ratios and higher WRs than HCM subjects without coronary spasm (P < 0.05, respectively). In conclusion, impaired sympathetic nerve function may be associated with coronary vasospasm and diminished coronary blood flow reserve in HCM. © 2007 Pulsus Group Inc. All rights reserved.
  • 118)早朝高血圧とメタボリックシンドローム(第102回日本循環器学会近畿地方会)
    環 愼二, 吉野 知秀, 松本 祐一, 高山 智行, 樽谷 康弘, 岡林 旅人, 川嶋 剛史, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • Churg-Strauss syndrome presenting with massive pericardial effusion
    Shinro Matsuo, Yuichi Sato, Tetsuya Matsumoto, Nobu Naiki, Minoru Horie
    Heart and Vessels 22(2) 128-130 2007年03月
    We describe a case of Churg-Strauss syndrome (CSS) presenting with a massive pericardial effusion without overt myocardial dysfunction. A 60-year-old man was referred to our hospital because of exertional dyspnea and fever. Initial chest multidetector-row computed tomography showed a massive pericardial effusion. The presence of eosinophilia, infiltrates of both lungs, pathological evidence of necrotizing vasculitis associated with eosinophilic infiltration, and history of asthma fulfilled the criteria of CSS. Massive pericardial effusion can be the first manifestation of cardiac involvement in CSS. © Springer-Verlag Tokyo 2007.
  • 126)急性心筋梗塞後チクロピジンにて血栓性血小板減少性紫斑病をきたした1例(第102回日本循環器学会近畿地方会)
    河原 千穂, 谷口 晋, 高島 弘行, 山本 孝, 松本 鉄也, 堀江 稔, 浜本 徹, 辻田 靖之, 江口 豊
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • Relationship between metabolic syndrome and Trp64Arg polymorphism of the β3-adrenergic receptor gene in a general sample: The Shigaraki study
    Shinji Tamaki, Yasuyuki Nakamura, Yasuharu Tabara, Tomonori Okamura, Yoshikuni Kita, Takashi Kadowaki, Yasuyuki Tsujita, Minoru Horie, Tetsuro Miki, Hirotsugu Ueshima
    Hypertension Research 29(11) 891-896 2006年11月
    It has been reported that the β3-adrenergic receptor gene (ADRB3) is associated with abnormal metabolic risk factors. Therefore, we examined whether the Trp64Arg polymorphism of ADRB3 affects the occurrence of metabolic syndrome (MS). The participants were 2,395 subjects who underwent a medical examination in Shigaraki in Shiga, Japan. Among them, 1,416 subjects who gave informed consent for genetic analysis and were not receiving treatment for hypertension, diabetes, or hyperlipidemia were enrolled in this study. MS was diagnosed in 86 (16.0%) of 537 men, and 8 (0.9%) of 879 women. Ther e was no significant relationship between ADRB3 polymorphism and the frequency of MS. Multiple logistic regression analysis including smoking, sex, and age as confounding factors showed no interaction between MS and ADRB3 polymorphism (odds ratio: 0.94; 95% confidence interval: 0.59-1.49; p=0.78). Subjects were also analyzed according to differences in the number of abnormal metabolic risk factors. However, there was no significant relationship between ADRB3 polymorphism and the number of such factors. In conclusion, in a general sample, the frequency of MS as 16.0% in men, and 0.9% in women. There was no relationship between ADRB3 polymorphism and MS.
  • 132)妊娠12週で急性大動脈解離を発症したMarfan症候群の一例(第102回日本循環器学会近畿地方会)
    寺村 真範, 高橋 聡文, 藤井 応理, 松本 鉄也, 堀江 稔, 四方 寛子, 野田 洋一, 辻田 靖之, 浜本 徹, 江口 豊
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • Response to letter regarding article, "angiotensin II potentiates the slow component of delayed rectifier K+ current via the AT1 receptor in guinea pig atrial myocytes" [2]
    Dimitar P. Zankov, Mariko Omatsu-Kanbe, Futoshi Toyoda, Wei Guang Ding, Hiroshi Matsuura, Takahiro Isono, Minoru Horie
    Circulation 114(18) 566 2006年10月
  • 161)急性心不全をきっかけに判明した右冠動脈肺動脈起始症の一例(第102回日本循環器学会近畿地方会)
    羽野 嘉文, 岡林 旅人, 吉野 知秀, 松本 祐一, 高山 智行, 樽谷 康弘, 環 信二, 川嶋 剛史, 山本 孝, 堀江 稔
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • Primary malignant lymphoma of the right atrium resulting in superior vena caval syndrome in an HIV-positive patient: depiction at multislice computed tomography and magnetic resonance imaging
    Shinro Matsuo, Yuichi Sato, Akashi Miyamoto, Ichiro Nakae, Michio Saeki, Keiko Hodohara, Minoru Horie
    Cardiovascular Revascularization Medicine 7(4) 255-257 2006年10月
    An HIV-positive 32-year-old male presenting with superior vena cava syndrome underwent multislice computed tomography (MSCT) and magnetic resonance imaging (MRI), which showed a large tumor in the right atrium, which extended to the superior vena cava. Pathologic examination revealed that the mass was consistent with B cell-type malignant lymphoma. The tumor size markedly decreased after the initiation of chemotherapy and patient recovery has been uneventful for 1 year. © 2006 Elsevier Inc. All rights reserved.
  • Novel mutation of plakophilin-2 associated with arrhythmogenic right ventricular cardiomyopathy
    Iori Nagaoka, Keiji Matsui, Takeshi Ueyama, Masashi Kanemoto, Jie Wu, Akihiko Shimizu, Masunori Matsuzaki, Minoru Horie, Minoru Horie
    Circulation Journal 70(7) 933-935 2006年07月
    Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disease characterized by dilatation and akinesis of the right ventricle, and causes life-threatening ventricular arrhythmia. Mutations of plakophilin-2 (PKP2) have recently been identified as one causative abnormality in ARVC. A case of ARVC with a mutation of PKP2 is reported here. Direct sequencing of the patient's DNA revealed an insertion mutation in exon 8 of PKP2 (1728_1729insGATG). The mutation caused the frameshift and the premature termination of translation (R577DfsX5). This is the first case report of PKP2 mutation found in Japanese ARVC patients.
  • alpha-Adducin gene
    Shinji Tamaki, Yasuyuki Nakamura, Minoru Horie, Masahiko Kinoshita, Naoharu Iwai
    Nippon rinsho. Japanese journal of clinical medicine. 64 Suppl 5 348-352 2006年07月
  • Tumor necrosis factor-α inhibits the cardiac delayed rectifier K current via the asphingomyelin pathway
    Katsuharu Hatada, Takashi Washizuka, Minoru Horie, Hiroshi Watanabe, Fumio Yamashita, Masaomi Chinushi, Yoshifusa Aizawa
    Biochemical and Biophysical Research Communications 344(1) 189-193 2006年05月
    Tumor necrosis factor-α (TNF-α) affects contractility and ionic currents in the heart. However, the electrophysiological effects, especially on delayed rectifier K currents (IK), have not yet been fully elucidated. We examined the effects of TNF-α on IK. Using a voltage-clamp method, IK was measured in guinea pig ventricular myocytes in the basal state and after pharmacological intervention. To specify the site of the action of TNF-α, the myocytes were incubated with pertussis toxin or N-oleoylethanolamine, a ceramidase inhibitor, and IK was measured. TNF-α suppressed IK when it was enhanced by isoproterenol, histamine or forskolin but not in the basal state or when IK was augmented by an internal application of cyclic AMP. Both pre-incubation with pertussis toxin and N-oleoylethanolamine abolished the inhibitory action of TNF-α on isoproterenol-augmented IK. TNF-α inhibits IK, mainly IKs, when it is augmented by PKA as a result of the generation of sphingosine. © 2006 Elsevier Inc. All rights reserved.
  • Scintigraphic evaluation of cardiac metabolism and sympathetic nerve function in alcoholic cardiomyopathy
    Shinro Matsuo, Ichiro Nakae, Daisuke Masuda, Tetsuya Matsumoto, Minoru Horie
    Internal Medicine 45(7) 465-467 2006年05月
    A 70-year-old man with alcoholic cardiomyopathy underwent 99m technetium-sestamibi (MIBI), iodine-123-labeled metaiodobenzylguanidine (MIBG) scintigraphy and Iodine-123-labeled beta-methyl-iodophenyl pentadecanoic acid (BMIPP) scintigraphy. 99m Technetium-MIBI identified myocardial damage in the inferior wall of left ventricle. 123 I BMIPP showed low uptake in the inferior wall of the myocardium, concordant to perfusion. 123 I BMIPP and 123 I MIBG showed reduced uptake in the inferior segment of the myocardium, indicating impairment of fatty acid metabolism and sympathetic abnormalities. Damaged myocardium was demonstrated in alcoholic cardiomyopathy. Beta blocker (carvedilol) and angiotensin-receptor blocker (valsartan) were started at low doses, then increased gradually, leading to the improvement of cardiac performance. Cardiac sympathetic nerve function, impaired due to alcoholic cardiomyopathy, was improved with beta-blocker therapy. Cardiac scintigraphy may be useful to assess the extent of myocardial improvement and the response to therapy. © 2006 The Japanese Society of Internal Medicine.
  • The Jervell and Lange-Nielsen syndrome: Natural history, molecular basis, and clinical outcome
    Peter J. Schwartz, Peter J. Schwartz, Peter J. Schwartz, Carla Spazzolini, Lia Crotti, Lia Crotti, Jørn Bathen, Jan P. Amlie, Katherine Timothy, Maria Shkolnikova, Charles I. Berul, Charles I. Berul, Maria Bitner-Glindzicz, Lauri Toivonen, Minoru Horie, Eric Schulze-Bahr, Eric Schulze-Bahr, Isabelle Denjoy, Isabelle Denjoy, Isabelle Denjoy
    Circulation 113(6) 783-790 2006年02月
    Background - Data on the Jervell and Lange-Nielsen syndrome (J-LN), the long-QT syndrome (LQTS) variant associated with deafness and caused by homozygous or compound heterozygous mutations on the KCNQ1 or on the KCNE1 genes encoding the I Ks current, are still based largely on case reports. Methods and Results - We analyzed data from 186 J-LN patients obtained from the literature (31%) and from individual physicians (69%). Most patients (86%) had cardiac events, and 50% were already symptoma tic by age 3. Their QTc was markedly prolonged (557±65 ms). Most of the arrhythmic events (95%) were triggered by emotions or exercise. Females are at lower risk for cardiac arrest and sudden death (CA/SD) (hazard ratio, 0.54; 95% CI, 0.34 to 0.88; P=0.01). A QTc > 550 ms and history of syncope during the first year of life are independent predictors of subsequent CA/SD. Most mutations (90.5%) are on the KCNQ1 gene; mutations on the KCNE1 gene are associated with a more benign course. β-Blockers have only partial efficacy; 51% of the patients had events despite therapy and 27% had CA/SD. Conclusions - J-LN syndrome is a most severe variant of LQTS, with a very early onset and major QTc prolongation, and in which β-blockers have limited efficacy. Subgroups at relatively lower risk for CA/SD are identifiable and include females, patients with a QTc ≤550 ms, those without events in the first year of life, and those with mutations on KCNE1. Early therapy with implanted cardioverter/defibrillators must be considered. © 2006 American Heart Association, Inc.
  • Recent topics on diagnosis and therapy for arrhythmia
    Minoru Horie
    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine 95(3) 520-523 2006年01月
  • Arrhythmia and the pathogenetic gene
    Hideki Ito, Minoru Horie
    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine 95(2) 203-208 2006年01月
  • Inhibition of aldosterone and endothelin-1 by carperitide was attenuated with more than 1 week of infusion in patients with congestive heart failure
    Chitose Ishikawa, Takayoshi Tsutamoto, Atsuyuki Wada, Masanori Fujii, Keijin Ohno, Hiroshi Sakai, Takashi Yamamoto, Minoru Horie
    Journal of Cardiovascular Pharmacology 46(4) 513-518 2005年10月
    Short-term infusion of carperitide (atrial natriuretic peptide) has beneficial effects on neurohumoral factors; however, it remains unclear whether the effects are sustained for long-term infusion. To evaluate the effects of long-term infusion of carperitide on neurohumoral factors in patients with chronic congestive heart failure (CHF), we measured neurohumoral factors before and 1 hour after stopping carperitide infusion in 42 CHF patients. Carperitide infusion was continued for more than 2 days until there was symptomatic improvement of CHF. Patients were divided into 2 groups by the median value of infusion duration: group 1 (less than 7 days, n = 21) and group 2 (more than 7 days, n = 21). In group 1, aldosterone (ALD) and endothelin-1 (ET-1) were significantly increased after stopping carperitide. In contrast, ALD and ET-1 did not change after stopping carperitide in group 2. The molar ratio of cyclic guanosine monophosphate/atrial natriuretic peptide before stopping carperitide was significantly lower in group 2 than in group 1. Suppression of ALD and ET-1 was maintained for 7 days of carperitide infusion, but the beneficial effect on neurohumoral factors was attenuated after more than 7 days, probably through down-regulation of biologic receptors coupled with guanylate cyclase in CHF patients. Copyright © 2005 by Lippincott Williams & Wilkins.
  • Left ventricular systolic/diastolic function evaluated by quantitative ECG-gated SPECT: Comparison with echocardiography and plasma BNP analysis
    Ichiro Nakae, Ichiro Nakae, Shinro Matsuo, Terue Koh, Kenichi Mitsunami, Minoru Horie
    Annals of Nuclear Medicine 19 447-454 2005年09月
    Objective: The aim of this study was to evaluate the left ventricular (LV) functional parameters calculated using quantitative electrocardiography (ECG)-gated myocardial perfusion single photon emission computed tomography (QGS). In addition to LV systolic parameters, diastolic parameters were compared with those by ultrasound echocardiography (UCG) and also with plasma B-type natriuretic peptide (BNP) concentrations. Methods: We examined 46 patients with various forms of heart disease. By the QGS data with 16 framing data acquisition using technetium (Tc)-99m methoxyisobutylisonitrile (MIBI) perfusion, we calculated the following parameters: LV end-diastolic volume (EDV), end-systolic volume (ESV), ejection fraction (EF), peak filling rate (PFR), filling rate during the first third of the filling time (1/3FR) and first third filling fraction (1/3FF). By UCG, we measured mitral early to atrial (E/A) wave velocity ratio and pulmonary venous inflow systolic/diastolic (S/D) ratio as diastolic functional parameters. Plasma BNP concentrations were also measured. Results: There was a significant correlation between LVEDV, ESV and EF measured by QGS and UCG (EDV, r = 0.71, p < 0.001; ESV, r = 0.82, p < 0.001 ; EF, r = 0.75, p < 0.001). The PFR, 1/3FR and 1/3FF obtained by QGS correlated positively with E/A ratio (PFR, r = 0.54, p < 0.001; 1/3FR, r = 0.61, p < 0.001; 1/3FF, r = 0.42, p < 0.01) and negatively with S/D ratio (PFR, r = -0.40, p < 0.01; 1/3FR, r = -0.38, p < 0.05; 1/3FF, r = -0.39, p < 0.01) obtained by UCG. Plasma BNP concentrations in EF < 50% patients were greater than those in EF ≥ 50% patients (335.2 ± 60.2 vs. 101.2 ± 41.3 pg/ml, p < 0.01, both n = 17). Plasma BNP levels were also compared between higher and lower 1/3FF patients matched for LVEF. Plasma BNP concentrations in 1/3FF < 35% patients were significantly greater than those in 1/3FF > 35% patients (312.9 ± 62.5 vs. 120.5 ± 32.8 pg/ml, p < 0.05, both n = 14). Conclusions: The degree of LV systolic and diastolic dysfunctions evaluated by QGS correlated with that by UCG or BNP. The QGS functional parameters offer useful information regarding cardiac failure.
  • Clinical significance of plasma BNP measurement in patients with pychiatric disease
    Ichiro Nakae, Shinro Matsuo, Terue Koh, Kenichi Mitsunami, Minoru Horie
    International Medical Journal 12 181-184 2005年09月
    Objective: Plasma BNP concentration is a useful marker of cardiac dysfunction which reflects the disease severity. It has been reported that antipsychotic agent may cause fatal cardiac complications along with QT prolongation on electrocardiogram. To investgate potentially progressive cardiac complications by antipsychotic agents, we examined plasma BNP concentrations in schizophrenic patients. Design: A clinical study. Methods: Plasma BNP concentrations in 60 inpatients with schizophrenia were examined. All patients were treated with antipsychotic agents for more than 1 year. The patients with cardiac disease, hypertension, renal dysfunction or diabetes mellitus were excluded. Results: Plasma BNP concentrations were significantly higher in schizophrenic patients than in age-matched normal controls (25.0 ± 56.8 vs 13.1 ± 11.2 pg/ml, p < 0.05). In 5 patients who exhibited higher plasma BNP concentrations, echocardiography failed to detect the abnormality of left ventricular dimension or systolic function. However, plasma BNP concentration correlated positively with the QT interval corrected for heart rate (QTc), suggesting cardiac alteration by antipsychotic agents. Conclusions: Our study suggests that cardiac complications may be potentially advanced in patients treated with antipsychotic agents. The measurement of plasma BNP may be useful for detecting cardiac complications in the early stage. © 2005 Japan International Cultural Exchange Foundation.
  • Combined analysis of polymorphisms in angiotensinogen and adducin genes and their effects on hypertension in a Japanese sample: The Shigaraki study
    Shinji Tamaki, Yasuyuki Nakamura, Yasuharu Tabara, Tomonori Okamura, Yoshikuni Kita, Takashi Kodawaki, Yasuyuki Tsujita, Minoru Horie, Tetsuro Miki, Hirotsugu Ueshima
    Hypertension Research 28(8) 645-650 2005年08月
    We examined the interactions between lifestyle and polymorphisms of salt-sensitive genes and their effects on hypertension in a general Japanese sample (The Shigaraki Study). The study group consisted of 2,902 subjects who underwent a medical examination in 1999 in Shigaraki, a suburban area in Shiga. Among 1,647 subjects not receiving antihypertensive medication, in a combined analysis of angiotensinogen (AGT) and adducin (ADD1) polymorphisms, double homozygosity of 235Trp or 460Trp was not found to be associated with hypertension. A multiple logistic regression analysis showed that age (odds ratio [OR]: 1.07, 95% confidence interval [95% CI] : 1.06-1.08), body mass index (BMI) (OR: 1.18, 95% CI: 1.13-1.23), alcohol consumption (OR: 1.39, 95% CI: 1.16-1.66), family history of hypertension (OR: 1.57, 95% CI: 1.18-2.07), and combined AGT M235T Thr/Thr and ADD1 Trp/Trp polymorphisms (OR: 1.37, 95% CI: 1.03-1.82) were associated with hypertension. However, there was no interaction between eating salty food and combined AGT and ADD1 polymorphisms. Furthermore, eating salty food was not associated with hypertension in a multivariate analysis. Therefore, a combination of the AGT and ADD1 polymorphisms appears to be associated with hypertension. However, a sim ple questionnaire regarding salt intake was not sufficient to confirm the relationship between salt intake and hypertension and/or salt-sensitive genes.
  • フォーラム 遺伝性不整脈疾患--その診断と治療
    堀江 稔
    セフィーロ(3) 75-78 2006年
  • Effect of statin therapy on arterial stiffness in patients with hyperlipidemia: Shiga pravastatin atherosclerosis study (SHIPAS) group
    Shinro Matsuo, Yasuyuki Nakamura, Tetsuhiro Yamada, Yasukazu Uchida, Ichiro Nakae, Minoru Horie
    Journal of Applied Research 5 397-401 2005年07月
    A man is as old as his arteries and the vascular remodeling is a common problem in the elderly. Aortic pulse wave velocity (PWV) provides noninvasive measurement of the mechanical properties of arteries. Objective: We measured the effects of HMA-CoA inhibitor (pravastatin) on arterial stiffness, ankle brachial index, PWV, and blood pressure (BP) in patients with hyperlipidemia. Design and Methods: The present study involved 15 patients (mean age 65 ± 2.7 years) with hyperlipidemia who were not on any medication. Aortic pulse wave velocity was evaluated at baseline and following 3 months of drug intake (pravastatin 10 mg/day). Twenty healthy volunteers constituted a control group. Results: Following 6 months of conventional treatments of hyperlipidemia, brachial systolic BP and diastolic BP did not change significantly with pravastatin from baseline (Not significant; NS). The PWV decreased significantly after treatment with pravastatin (1912 ± 90.3 vs 1755 ± 96.9 cm/sec, P < 0.001). There was no significant difference in control subjects (1677 ± 71.5 vs 1796 ± 56 cm/sec. NS). The decrease in PWV with pravastatin was independent of blood pressure (P < 0.05). Conclusions: The study shows that HMA-CoA inhibitor might improve arterial wall stiffness in patients with hyperlipidemia.
  • Electrocardiographic features in Andersen-Tawil syndrome patients with KCNJ2 mutations: Characteristic T-U-wave patterns predict the KCNJ2 genotype
    Li Zhang, Li Zhang, D. Woodrow Benson, Martin Tristani-Firouzi, Louis J. Ptacek, Rabi Tawil, Peter J. Schwartz, Alfred L. George, Minoru Horie, Gregor Andelfinger, Gregory L. Snow, Ying Hui Fu, Michael J. Ackerman, G. Michael Vincent, G. Michael Vincent, G. Michael Vincent
    Circulation 111(21) 2720-2726 2005年05月
    Background - The ECG features of Andersen-Tawil syndrome (ATS) patients with KCNJ2 mutations (ATS1) have not been systematically assessed. This study aimed to define ECG features of KCNJ2 mutation carriers, to determine whether characteristic T-U-wave patterns exist, and to establish whether T-U patterns predict the ATS1 genotype. Methods and Results - In phase I, evaluation of T-U morphology in ECGs of 39 KCNJ2 mutation carriers identified characteristic T-U patterns: prolonged terminal T downslope, wide T-U junction, and biphasic and enlarged U waves. In phase II, ATS1 genotype prediction by T-U pattern was evaluated in the next 147 ECGs (57 other KCNJ2 mutation carriers, 61 unaffected family members, and 29 ATS patients without KCNJ2 mutations), with a sensitivity of 84% and specificity of 97%. Characteristic T-U patterns were present in 91% (87/96), in whom an enlarged U wave was predominant (73%). In phase III, QTc, QUc, and T- and U-wave duration/amplitude were compared in the 96 ATS1, 29 non-KCNJ2 ATS, and 75 normal subjects. In ATS1 patients, QUc, U-wave duration and amplitude, and QTc were all increased (P < 0.001), but median QTc and interquartile range (IQR) were just 440 ms (IQR, 28 ms) compared with 420 ms (IQR, 20 ms) in normal subjects and 425 ms (IQR, 48 ms) in ATS non-KCNJ2 patients. Conclusions - In ATS1 patients, gene-specific T-U-wave patterns resulting from decreased I K1 owing to KCNJ2 mutations can aid diagnosis and direct genotyping. The normal QTc, distinct ECG, and other clinical features distinguish ATS1 from long-QT syndrome, and it is best designated as ATS1 rather than LQT7. © 2005 American Heart Association, Inc.
  • Detection of calf muscle alterations in patients with chronic heart failure by 31P magnetic resonance spectroscopy: Impaired adaptation to continuous exercise
    Ichiro Nakae, Kenichi Mitsunami, Shinro Matsuo, Toshiro Inubushi, Shigehiro Morikawa, Terue Koh, Minoru Horie
    Experimental and Clinical Cardiology 10 4-8 2005年05月
    Previous studies suggested that alteration of systemic skeletal muscle metabolism is a major determinant of exercise tolerance in patients with chronic heart failure (CHF). The authors examined calf muscle metabolism during continuous exercise of the foot in patients with CHF compared with normal subjects using 31 p magnetic resonance spectroscopy. The subjects were patients with New York Heart Association class II CHF who had previously suffered New York Heart Association class IV heart failure. Plantarflexion of the foot was repeated for 8 min 40 s at a rate of one contraction per second against a 2 kg load inside the magnet. At rest, during exercise (divided into the first one-half [EX1] and the latter one-half [EX2] ) and at recovery, 31 p magnetic resonance spectroscopy data sets were acquired every 4 min 20 s. At rest, the phosphocreatine to hexamethylphosphoric triamide (PCr:HMPT) and the inorganic phosphate (Pi) to PCr ratios in the CHF group were not different from those in the normal group. During EX1 in the normal group, PCr levels decreased and Pi levels increased. Although exercise continued, these changes improved during EX2, suggesting there was an adaptation to exercise. The degree of change in the PCr:HMPT ratio during EX1 in the CHF group was not significantly different from that during EX1 in the normal group; however, the improvement during EX2 in the CHF group was impaired. The Pi:PCr ratio of EX1 to EX2 in the CHF group was significantly greater than that in the normal group (0.74±0.22 versus 0.19±0.05, respectively, P < 0.005). Thus, in CHF, adaptation to continuous exercise may be impaired by alteration of skeletal muscle metabolism and this alteration may worsen exercise capacity. © 2005 Pulsus Group Inc. All rights reserved.
  • Dilated cardiomyopathy relieved as a result of β-blocker therapy: A case report - Key points in assessment of prognosis based on MIBG myocardial scintigraphy and BNP levels
    Shinro Matsuo, Shinro Matsuo, Ichiro Nakae, Daisuke Masuda, Tetsuya Matsumoto, Minoru Horie
    Annals of Nuclear Medicine 19(3) 243-246 2005年05月
    A 48-year-old male patient was admitted to our hospital with dyspnea accompanied by orthopnea. Chest x-rays showed a cardiothoracic ratio of 68% and pulmonary congestion. He was diagnosed with dilated cardiomyopathy. β-Blocker (carvedilol) therapy was initiated on Day 22 of the disease using a small initial dose. He was followed up based on BNP levels and MIBG scintigraphy. The H/M ratio and MIBG washout rate were 1.98 and 33.4%, respectively, on Day 20 and 2.15 and 28.1%, respectively, on Day 72. The patient was discharged on Day 72 when congestive heart failure improved. Relatively high BNP levels were observed for 1 month after starting treatment with a β-blocker. Plasma BNP levels were still as high when his heart failure was improved. BNP is useful as a convenient indicator for the severity of cardiac diseases. MIBG scintigraphy may be used thereafter to evaluate the severity in greater detail and more precisely determine the prognosis.
  • Regulation of the muscarinic K + channel by extracellular ATP through membrane phosphatidylinositol 4,5-bisphosphate in guinea-pig atrial myocytes
    Yoh Yasuda, Yoh Yasuda, Hiroshi Matsuura, Makoto Ito, Tetsuya Matsumoto, Wei Guang Ding, Minoru Horie
    British Journal of Pharmacology 145(2) 156-165 2005年05月
    The present study was designed to examine the functional role of membrane phosphatidylinositol 4,5-bisphosphate (PtdIns(4,S)P 2 ) in the regulation of the muscarinic K + channel (I K.ACh ) by extracellular ATP and adenosine in guinea-pig atrial myocytes, using the whole-cell patch-clamp method. Bath application of ATP in micromolar concentrations typically evoked a transient activation of I K.ACh ; a rapid activation phase was consistently followed by a progressive decline even to the baseline level despite the continued presence of ATP. This progressive decline of I K.ACh was significantly attenuated either by blockade of phospholipase C (PLC) with compound 48/80 (100 μM) or by addition of PtdIns(4,5)P 2 (50 μM) to the cell inside, suggesting that depletion of membrane PtdIns(4,5)P 2 via PLC activation is mainly, if not totally, responsible for the progressive decline of I K.ACh during the presence of ATP. When atrial myocytes were exposed to wortmannin (50 μM) following ATP (50 μM) application to impair the resynthesis of PtdIns(4,5)P 2 , the activation of I K.ACh evoked by subsequently applied ATP (50 μM) was greatly reduced. Activation of I K.ACh by adenosine (100 μM) was partially reduced by pretreatment of atrial myocytes with ATP (100 μM) and was largely abolished by a further addition of wortmannin (50 μM) in the presence of ATP (100 μM). These results support the view that the activation of I K.ACh by ATP and adenosine depends on membrane PtdIns(4,5)P 2 that is subject to reduction by extracellular ATP. The present study thus provides functional evidence to suggest that extracellular ATP activates PLC and thereby depletes membrane PtdIns(4,5)P 2 that is critically involved in the activation process of I K.ACh by its agonists ATP and adenosine in guinea-pig atrial myocytes. © 2005 Nature Publishing Group. All rights reserved.
  • Double SCN5A mutation underlying asymptomatic Brugada syndrome
    Hisataka Yokoi, Naomasa Makita, Koji Sasaki, Yasuhiro Takagi, Yasuo Okumura, Tetsuo Nishino, Takeru Makiyama, Akira Kitabatake, Minoru Horie, Ichiro Watanabe, Hiroyuki Tsutsui
    Heart Rhythm 2(3) 285-292 2005年03月
    Objectives: The purpose of this study was to identify risk markers in patients with Brugada syndrome. Background: Patients with Brugada syndrome who experience syncope or aborted sudden death are at high risk for recurrent lethal arrhythmias. The prognosis and therapeutic approaches in asymptomatic individuals with a Brugada-type ECG (asymptomatic Brugada syndrome) are controversial. Methods: We genetically screened 30 asymptomatic probands (29 men and 1 woman; mean age 47.1 years) exhibiting a spontaneous Brugada-type ECG. Family members of patients with Brugada syndrome were excluded from the study. Results: Twenty-nine of 30 patients (96.7%) remained symptom-free for at least 3 years. One patient (case 1) with a family history of sudden death died suddenly during sleep. Ventricular fibrillation was induced by programmed electrical stimulation in 14 of 18 subjects (78%), but none of these 18 subjects developed spontaneous ventricular arrhythmias. Genetic screening failed to identify SCN5A mutations in most cases but demonstrated a novel double missense mutation (K1527R and A1569P) located on the same allele in another asymptomatic subject (case 2). Heterologously expressed mutant Na channels exhibited a negative shift of steady-state inactivation (9.2 mV) and enhanced slow inactivation, suggesting this individual harbors a subclinical channel dysfunction compatible with symptomatic Brugada syndrome. Conclusions: Asymptomatic individuals with a Brugada-type ECG generally have a better prognosis than their symptomatic counterparts, but a subgroup of these individuals may have a poor prognosis. Severe Na channel dysfunction as a result of SCN5A mutations may not be sufficient to cause symptoms or arrhythmias in patients with Brugada syndrome, suggesting unknown factors or modifier genes influence arrhythmogenesis. © 2005 Heart Rhythm Society. All rights reserved.
  • Noninvasive evaluation of coronary artery plaque with electrocardiographically-gated multislice computed tomography
    Shinro Matsuo, Ichiro Nakae, Tetsuya Matsumoto, Minoru Horie
    CMIGExtra: Cases 29(2) 13-18 2005年03月
    The study evaluated the feasibility of determining coronary lesion configuration, including coronary plaque, stenosis and calcification, by ECG-gated MSCT. The results were compared with the characteristics of intravascular ultrasound (IVUS). The overall sensitivity for diagnosing significant coronary stenosis was 80.2%, and the specificity was 95.6%. There were significant differences in plaque density among three groups (p < 0.01). MSCT was feasible for the detection of coronary artery stenosis. And plaque composition could be clearly differentiated and classified by MSCT, which is a promising method of non-invasive risk assessment in patients with known or suspected coronary artery disease. © 2005 Elsevier Ltd. All rights reserved.
  • Brachial artery flow-mediated vasodilation is correlated with coronary vasomotor and fibrinolytic responses induced by bradykinin
    Yasuhiro Tarutani, Tetsuya Matsumoto, Hiroyuki Takashima, Tetsunobu Yamane, Minoru Horie
    Hypertension Research 28(1) 59-66 2005年01月
    Endothelium plays a key role in the regulation of not only vascular tone but also thrombosis and fibrinolysis. Brachial flow-mediated vasodilation (FMD) provides a noninvasive method of assessing coronary endothelial dysfunction. However, no data are available on the relationship between brachial FMD and coronary fibrinolytic activity. Thus, we examined the relationship between brachial FMD and coronary vasomotor and fibrinolytic function. Brachial FMD by reactive hyperemia was defined as a change in diameter relative to the baseline as measured using high-resolution ultrasound. Coronary blood flow (CBF) responses to bradykinin (BK) were analyzed using Doppler flow velocity measurement. Coronary release of tissue-type plasminogen activator (tPA) antigen was determined as the transcardiac tPA gradient × {CBF × (100 - hematocrity)/100}. In 77 patients with normal coronary arteries, BK caused dose-dependent increases in CBF, transcardiac tPA gradient, and coronary tPA release. Among them, brachial FMD, the BK-induced CBF increase, and the coronary tPA release induced by BK in 14 diabetic subjects were lower than those in 63 non-diabetic subjects (p < 0.05, respectively). Brachial FMD correlated with the CBF increase, transcardiac tPA gradient (0.2 μg/min: r=0.25; 0.6 μg/min: r=0.43; 2.0 μg/min: r=0.34; p < 0.05, respectively), and coronary tPA release (0.2 μg/min: r=0.24; 0.6 μg/min: r=0.44; 2.0 μg/min: r=0.32; p < 0.05, respectively) in response to BK. Brachial FMD correlated significantly with coronary endothelial function and fibrinolytic activity in response to BK. Type 2 diabetes impaired coronary and brachial endothelium-dependent vasodilation and coronary fibrinolytic activity.
  • Diagnosis of heart failure by measuring humoral factors
    Takayoshi Tsutamoto, Minoru Horie
    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine 94 221-227 2005年01月
  • Cardiovascular imaging by means of multi-slice CT in cardiology.
    Shinro Matsuo, Minoru Horie
    Nippon Hoshasen Gijutsu Gakkai zasshi 61 1309-1317 2005年01月
  • Left ventricular remodeling post myocardial infarction
    Takayoshi Tsutamoto, Minoru Horie, Masaru Hayashi
    Nippon rinsho. Japanese journal of clinical medicine 63 Suppl 3 323-329 2005年01月
  • In situ Ca2+dynamics of Purkinje fibers and its interconnection with subjacent ventricular myocytes
    Tetsu Hamamoto, Tetsu Hamamoto, Hideo Tanaka, Hiroki Mani, Takuji Tanabe, Katsuji Fujiwara, Takuo Nakagami, Minoru Horie, Masahito Oyamada, Tetsuro Takamatsu
    Journal of Molecular and Cellular Cardiology 38(4) 561-569 2005年01月
    Purkinje fibers play essential roles in impulse propagation to the ventricles, and their functional impairment can become arrhythmogenic. However, little is known about precise spatiotemporal pattern(s) of interconnection between Purkinje-fiber network and the underlying ventricular myocardium within the heart. To address this issue, we simultaneously visualized intracellular Ca 2+ dynamics at Purkinje fibers and subjacent ventricular myocytes in Langendorff-perfused rat hearts using multi-pinhole type, rapid-scanning confocal microscopy. Under recording of electrocardiogram at room temperature spatiotemporal changes in fluo3-fluorescence intensity were visualized on the subendocardial region of the right-ventricular septum. Staining of the heart with either fluo3, acetylthiocholine iodide (ATCHI), or di-4-ANEPPS revealed characteristic structures of Purkinje fibers. During sinus rhythm (about 60 bpm) or atrial pacing (up to 3 Hz) each Purkinje-fiber exhibited spatiotemporally synchronous Ca 2+ transients nearly simultaneously to ventricular excitation. Ca 2+ transients in individual fibers were still synchronized within the Purkinje-fiber network not only under high-K + (8 mM) perfusion-induced Purkinje-to-ventricular (P-V) conduction delay, but also under unidirectional, orthodromic P-V block produced by 10-mM K + perfusion. While spontaneous, asynchronous intracellular Ca 2+ waves were identified in injured fibers of Purkinje network locally, surrounding fibers still exhibited Ca 2+ transients synchronously to ventricular excitation. In summary, these results are the first demonstration of intracellular Ca 2+ dynamics in the Purkinje-fiber network in situ. The synchronous Ca 2+ transients, preserved even under P-V conduction disturbances or under emergence of Ca 2+ waves, imply a syncytial role of Purkinje fibers as a specialized conduction system, whereas unidirectional block at P-V junctions indicates a substrate for reentrant arrhythmias. © 2005 Elsevier Ltd. All rights reserved.
  • Torasemide inhibits transcardiac extraction of aldosterone in patients with congestive heart failure [3]
    Takayoshi Tsutamoto, Hiroshi Sakai, Atsuyuki Wada, Chitose Ishikawa, Keijin Ohno, Masanori Fujii, Takashi Yamamoto, Tomoyuki Takayama, Tomohiro Dohke, Minoru Horie
    Journal of the American College of Cardiology 44(11) 2252-2253 2004年12月
  • Evaluation of cardiac resynchronization therapy in drug-resistant idiopathic dilated cardiomyopathy by means of technetium-99m tetrofosmin electrocardiography-gated single-photon emission computed tomography
    Shinro Matsuo, Tetsuya Matsumoto, Ichiro Nakae, Makoto Ito, Yasuyuki Nakamura, Masahiko Takada, Kiyoshi Murata, Minoru Horie
    Experimental and Clinical Cardiology 9 248-250 2004年12月
    The present case report describes a 72-year-old woman with drug-resistant heart failure. Cardiac resynchronization therapy was performed. Cardiac function was evaluated using a quantitative gated single-photon emission computed tomography (QGS) program with technetium-99m tetrofosmin. During atrial-right ventricular pacing, the left ventricular ejection fraction (LVEF) was 28%, end diastolic volume (EDV) was 141 mL and end systolic volume (ESV) was 101 mL. LVEF was 31%, EDV was 142 mL and ESV was 98 mL during dual chamber pacing. During atrial-left ventricular pacing, LVEF, EDV and ESV were 32%, 18 mL and 100 mL, respectively. Diastolic function was evaluated using Vcdiff software (Daiichi Radioisotope Laboratories Ltd, Japan). Cardiac resynchronization therapy may improve cardiac function, which was evaluated accurately and non-invasively by electrocardiography-gated single-photon emission computed tomography. © 2004 Pulsus Group Inc. All rights reserved.
  • Endogenous bradykinin suppresses myocardial fibrosis through the cardiac-generated endothelin system under chronic angiotensin-converting enzyme inhibition in heart failure
    Masanori Fujii, Atsuyuki Wada, Atsuyuki Wada, Masato Ohnishi, Takayoshi Tsutamoto, Takehiro Matsumoto, Takashi Yamamoto, Tomoyuki Takayama, Tomohiro Dohke, Takahiro Isono, Yutaka Eguchi, Minoru Horie
    Journal of Cardiovascular Pharmacology 44 346-349 2004年11月
    In congestive heart failure, angiotensin-converting enzyme inhibitors (ACEIs) may prevent cardiac fibrosis via interaction with both angiotensin II and endothelin-1, which enhance myocardial collagen synthesis. However, whether endogenous bradykinin with an ACEI modifies the cardiac collagen architecture, affecting the endothelin system, has not yet been fully elucidated. We evaluated the changes in circulating hormonal factors, myocardial fibrosis and cardiac gene expression closely linked with heart failure, using an orally active specific bradykinin type 2 receptor antagonist, FR173657 (0.3 mg/kg/day, n = 6), with an ACEI, enalapril (1 mg/kg/day), in dogs with tachycardia-induced congestive heart failure (270 p.p.m., 22 days) and compared the effects with enalapril alone (n = 6). Although there were no differences observed in blood pressure, plasma renin activity, aldosterone and endothelin-1 levels, combined FR173657 significantly increased the cardiac expression of preproendothelin-1 mRNA (P < 0.05) and collagen type I and type III mRNA (P < 0.05), and cardiac collagen deposits (P < 0.05), and decreased eNOS gene expression (P < 0.05) in the left ventricle compared with the ACEI-treated group. Furthermore, there was a significant negative correlation between the expression of preproendothelin-1 and eNOS mRNA levels (r = -0.708, P < 0.001). In conclusion, bradykinin may prevent cardiac fibrosis in part via suppression of the local endothelin system in the failing heart through the enhancement of nitric oxide production under chronic angiotensin-converting enzyme inhibition.
  • Long-term treatment with a phosphodiesterase type 5 inhibitor improves pulmonary hypertension secondary to heart failure through enhancing the natriuretic peptides-cGMP pathway
    Takashi Yamamoto, Atsuyuki Wada, Atsuyuki Wada, Takayoshi Tsutamoto, Masato Ohnishi, Minoru Horie
    Journal of Cardiovascular Pharmacology 44(5) 596-600 2004年11月
    In advanced heart failure (HF), the compensatory pulmonary vasodilation is attenuated due to the relative insufficiency of cGMP despite increased secretion of natriuretic peptides (NPs). Phosphodiesterase type 5 (PDE5) inhibitors prevent cGMP degradation, and thus may potentiate the effect of the NPs-cGMP pathway. We orally administered a specific PDE5 inhibitor, T-1032 (1 mg/kg; twice a day, n = 7) or placebo (n = 7) for 2 weeks in dogs with HF induced by rapid pacing (270 bpm, 3 weeks) and examined the plasma levels of atrial natriuretic peptide (ANP), cGMP, and hemodynamic parameters. We also examined the hemodynamic changes after injection of a specific NPs receptor antagonist, HS-142-1 (3 mg/kg), under treatment with T-1032. T-1032 significantly increased plasma cGMP levels compared with the vehicle group despite low plasma ANP levels associated with improvement in cardiopulmonary hemodynamics. HS-142-1 significantly decreased plasma cGMP levels in both groups, whereas it did not change all hemodynamic parameters in the vehicle group. In contrast, in the T-1032 group, HS-142-1 significantly increased pulmonary arterial pressure and pulmonary vascular resistance. These results indicated that long-term treatment with a PDE5 inhibitor improved pulmonary hypertension secondary to HF and the NPs-cGMP pathway contributed to this therapeutic effect.
  • Contribution of vascular NAD(P)H oxidase to endothelial dysfunction in heart failure and the therapeutic effects of HMG-CoA reductase inhibitor
    Tomoyuki Takayama, Atsuyuki Wada, Atsuyuki Wada, Takayoshi Tsutamoto, Masato Ohnishi, Masanori Fujii, Takahiro Isono, Minoru Horie
    Circulation Journal 68(11) 1067-1075 2004年11月
    Background: The vascular NAD(P)H oxidase-derived superoxide anion (O 2 -) plays a crucial role in the pathological progression of hypertension and atherosclerosis, and HMG-CoA reductase inhibitors (statins) have vascular antioxidant effects. However, it is unclear whether the vascular NAD(P)H oxidase is involved in the endothelial dysfunction of congestive heart failure (CHF) and whether HMG-CoA reductase inhibitors (statins) exert their vasoprotective effects in CHF. The present study examined both the involvement of vascular NAD(P)H oxidase in endothelial dysfunction in dogs with tachycardia-induced CHF and the therapeutic effect of a statin (pitavastatin). Methods and Results: Femoral blood flow (FBF) responses to acetylcholine was significantly impaired in the CHF group, but were improved by pitavastatin. Vascular O 2 - production, NAD(P)H oxidase activity and Nox4 and p47phox expression were significantly elevated in CHF compared with the normal group. The elevated O 2 -production in the CHF group was suppressed by the NAD(P)H oxidase inhibitor, apocynin, to the normal level. In contrast, neither the gene expression nor the activity of endothelial nitric oxide synthase (eNOS) differed significantly between the normal and CHF groups. However, pitavastatin significantly suppressed O 2 - production, NAD(P)H oxidase activity and Nox4 and p47phox expression and increased eNOS expression and activity compared with the CHF group. Conclusions: The activated vascular NAD(P)H oxidase contributes to endothelial dysfunction in CHF, which was partly improved by pitavastatin via its inhibition of NAD(P)H oxidase.
  • Antihypertensive therapy of morning blood pressure - ATOM study
    Shinji Tamaki, Masato Ohnishi, Minoru Horie, Satoshi Morimoto
    Japanese Pharmacology and Therapeutics 32 481-486 2004年10月
    Background: Several prospective studies have indicated that early morning hypertension and morning blood pressure (BP) surge are important risk factors of stroke or cardiovascular events. We investigated differences between early morning and clinic BP as well as morning BP surge in patients being treated for essential hypertension. Design: We recorded systolic BP at three different times 1) before going to bed and, 2) in the early morning period before visiting the clinic by self-measurement at home, and 3) while at the clinic. Results: Although 40.4% of all patients demonstrated normal systolic BP while at the clinic, 50.3% of those demonstrated early morning hypertension. Only 19.0% of the patients demonstrated normal systolic BP both at the clinic and in the early morning. The mean morning BP surge was 9.16 ± 16.9 mmHg. Those patients who had taken valsartan resulted a particularly large surge, and a significant difference was observed between candesartan. Conclusion: These findings suggest that a strategy for controlling BP must be considered not only clinic BP but also morning home BP, and that the duration of BP lowering effects varies between anti-hypertensive agents.
  • Detection of metabolic abnormality in asynergic regions of ischemic human myocardium using 31P and 1H magnetic resonance spectroscopy
    Ichiro Nakae, Kenichi Mitsunami, Kenichi Mitsunami, Takahiro Yabe, Toshiro Inubushi, Shigehiro Morikawa, Shinro Matsuo, Terue Koh, Minoru Horie
    Journal of Cardiovascular Magnetic Resonance 6(3) 685-696 2004年08月
    To assess quantitatively phosphocreatine (PCr), adenosine triphosphate (ATP) and total creatine (CR) in asynergic regions of ischemic human myocardium using phosphorus ( 31 P) and proton magnetic resonance spectroscopy ( 1 H MRS). Patients were divided into two groups: 31 P MRS and 1 H MRS. In each group, patients were subdivided into three groups using echocardiography: a normokinetic [WNP (n = 6) in 31 P MRS, WNH (n = 10) in 1 H MRS], a hypokinetic [WHP (n = 13), WHH (n = 7)] , and a- or dyskinetic wall motion groups [WAP (n = 14), WAH (n = 6)]. They were compared with normal subjects of each group [CNP (n = 10), CNH (n = 10)] . 31 P MRS spectra were obtained from the anterior and apical regions of the left ventricle by slice-selected 1D CSI. 1 H MRS spectra were obtained from the 2 x 2 x 2-cm voxel set in the left ventricular wall by the PRESS method. In the 31 P MRS group, myocardial PCr was significantly lower in the WHP and WAP groups than in the CNP group, but myocardial PCr in the WNP group did not differ from that in CNP. A difference in ATP could not be detected among the four groups. In the 1 H MRS group, myocardial CR was significantly lower in the WHH and WA. groups than in the CNH group. Myocardial CR in the WNH group did not differ from that in the CNH. The noninvasive 31 P and 1 H MRS approach is useful in the assessment of metabolite reduction associated with wall motion abnormality.
  • The relationship between flow-mediated brachial artery vasodilation and coronary vasomotor responses to bradykinin: Comparison with those to acetylcholine
    Shinro Matsuo, Tetsuya Matsumoto, Hiroyuki Takashima, Naoto Ohira, Tetsunobu Yamane, Yo Yasuda, Yasuhiro Tarutani, Minoru Horie
    Journal of Cardiovascular Pharmacology 44(2) 164-170 2004年08月
    Flow-mediated dilation (FMD) of brachial artery provides a noninvasive assessment of coronary endothelial dysfunction. Acetylcholine (ACh) has been used as an agent for estimating coronary endothelial function. In contrast to ACh, there is no evidence for a relationship between FMD and coronary vasodilation to bradykinin (BK). The aim of this study was to compare the flow-mediated vasodilation of brachial artery with coronary vasomotor responses to intracoronary ACh or BK in patients with an angiographically normal left anterior descending coronary artery. Ninety-one patients underwent the cardiac catheterization examination with coronary endothelial function testing and the brachial ultrasound study. BK (0.2, 0.6, 2.0 μg/min) and ACh (3, 10, 30 μg/min) were administered into the left coronary artery in a stepwise manner. Coronary blood flow was evaluated by the Doppler flow velocity measurement. Coronary diameters were measured by the quantitative coronary angiography. The assessment of endothelial function in the brachial artery was made in response to reactive hyperemia with high-resolution ultrasound. Bradykinin induced dose-dependent increases in epicardial coronary diameter and blood flow. There was a significant positive correlation between FMD- and BK-induced vasodilations of epicardial coronary arteries (0.2 μg/min: r = 0.30; 0.6 μg/min: r = 0.42; 2.0 μg/min: r = 0.44, P < 0.01, respectively) and resistance coronary arteries (0.2 μg/min: r = 0.40; 0.6 μg/min: r = 0.56; 2.0 μg/min: r = 0.59, P < 0.0001, respectively). FMD correlated with ACh-induced vasomotions of resistance but not epicardial coronary arteries. No correlation was seen between nitroglycerin-induced brachial artery vasodilation and BK-induced coronary vasodilation. The endothelial dysfunction of peripheral arteries correlated well with that of the coronary arteries especially vasomotor responses to BK.
  • Plasma level of oxidized low-density lipoprotein is an independent determinant of coronary macrovasomotor and microvasomotor responses induced by bradykinin
    Tetsuya Matsumoto, Tetsuya Matsumoto, Hiroyuki Takashima, Naoto Ohira, Yasuhiro Tarutani, Yo Yasuda, Tetsunobu Yamane, Shinro Matsuo, Minoru Horie
    Journal of the American College of Cardiology 44(2) 451-457 2004年07月
    Objectives We examined the relationship between coronary endothelium-dependent vasodilation in response to bradykinin (BK) and plasma levels of oxidized low-density lipoprotein (oxLDL) in subjects with normal coronary arteries. Background It is unclear whether the plasma oxLDL level is a determinant of coronary endothelial function. Bradykinin plays an important role in regulating resting coronary tone and flow-mediated coronary vasomotion. Methods Coronary blood flow (CBF) in the left anterior descending (LAD) coronary artery was assessed by quantitative angiography and a Doppler flow wire in 94 consecutive subjects with normal coronary arteries. The plasma oxLDL level was measured by enzyme-linked immunosorbent assay using DLH3R, a specific antibody against oxLDL. Results Plasma levels of oxLDL in diabetic subjects (n = 13) were higher than those in non-diabetic subjects (n = 81). Plasma levels of oxLDL correlated with body mass index (BMI). Bradykinin at doses of 0.2, 0.6, and 2.0 μg/min caused dose-dependent increases in diameter and CBF in the LAD coronary artery. By a univariate analysis, oxLDL levels significantly correlated with epicardial (r = -0.30, p < 0.0001) and resistant (r = -0.36, p = 0.003) coronary vasodilator responses to BK at 2.0 μg/min, whereas total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides were not associated with these coronary responses. In a stepwise multivariate analysis, oxLDL levels were significantly correlated with epicardial and resistant coronary vasomotor responses to BK, independent of age, gender, smoking status, other lipid levels, BMI, hypertension, and diabetes. Conclusions The plasma level of oxLDL is an appropriate surrogate for assessing coronary endothelial-dependent vasomotor function as estimated by responses to BK compared with conventional risk factors for atherosclerosis. © 2004 by the American College of Cardiology Foundation.
  • Mutation site-specific differences in arrhythmic risk and sensitivity to sympathetic stimulation in the LQT1 form of congenital long QT syndrome: Multicenter study in Japan
    Wataru Shimizu, Wataru Shimizu, Wataru Shimizu, Minoru Horie, Seiko Ohno, Kotoe Takenaka, Masato Yamaguchi, Masami Shimizu, Takashi Washizuka, Yoshifusa Aizawa, Kazufumi Nakamura, Tohru Ohe, Takeshi Aiba, Yoshihiro Miyamoto, Yasunao Yoshimasa, Jeffrey A. Towbin, Silvia G. Priori, Shiro Kamakura
    Journal of the American College of Cardiology 44(1) 117-125 2004年07月
    Objectives We sought to compare the arrhythmic risk and sensitivity to sympathetic stimulation of mutations located in transmembrane regions and C-terminal regions of the KCNQ1 channel in the LQT1 form of congenital long QT syndrome (LQTS). Background The LQT1 syndrome is frequently manifested with variable expressivity and incomplete penetrance and is much more sensitive to sympathetic stimulation than the other forms. Methods Sixty-six LQT1 patients (27 families) with a total of 19 transmembrane mutations and 29 patients (10 families) with 8 C-terminal mutations were enrolled from five Japanese institutes. Results Patients with transmembrane mutations were more frequently affected based on electrocardiographic (ECG) diagnostic criteria (82% vs. 24%, p < 0.0001) and had more frequent LQTS-related cardiac events (all cardiac events: 55% vs. 21%, p = 0.002; syncope: 55% vs. 21%, p = 0.002; aborted cardiac arrest or unexpected sudden cardiac death: 15% vs. 0%, p = 0.03) than those with C-terminal mutations. Patients with transmembrane mutations had a greater risk of first cardiac events occurring at an earlier age, with a hazard ratio of 3.4 (p = 0.006) and with an 8% increase in risk per 10-ms increase in corrected Q-Tend. The baseline ECG parameters, including Q-Tend, Q-Tpeak, and Tpeak-end intervals, were significantly greater in patients with transmembrane mutations than in those with C-terminal mutations (p < 0.005). Moreover, the corrected Q-Tend and Tpeak-end were more prominently increased with exercise in patient s with transmembrane mutations (p < 0.005). Conclusions In this multicenter Japanese population, LQT1 patients with transmembrane mutations are at higher risk of congenital LQTS-related cardiac events and have greater sensitivity to sympathetic stimulation, as compared with patients with C-terminal mutations. © 2004 by the American College of Cardiology Foundation.
  • Brain Natriuretic Peptide
    蔦本 尚慶, 堀江 稔
    臨床病理 52(8) 655-668 2004年08月
  • 164)救急隊による心肺蘇生と病病連携にて社会復帰しえたマラソン競技中の心肺停止の一例(第102回日本循環器学会近畿地方会)
    浜本 徹, 辻田 靖之, 江口 豊, 寺村 真範, 芦原 貴司, 伊藤 誠, 堀江 稔, 松本 祐一, 川嶋 剛史
    Circulation journal : official journal of the Japanese Circulation Society 71(0) 2007年04月
  • Scintigraphic evaluation of cardiac metabolism in multicentric Castleman's disease
    Shinro Matsuo, Yasuyuki Nakamura, Ichiro Nakae, Tetsuya Matsumoto, Masahiko Takada, Kiyoshi Murata, Minoru Horie
    Internal Medicine 43(6) 490-492 2004年06月
    A 72-year-old woman had insidious onset of heart failure, and was diagnosed as multicentric Castleman's disease. She underwent myocardial imaging with technetium-99m tetrofosmin, I-123 beta-methyl-iodophenyl pentadecanoic acid (BMIPP). Technetium-99m tetrofosmin studies showed almost normal uptake of the left ventricular myocardium indicating normal myocardial perfusion. I-123 BMIPP showed reduced uptake in the apical segment of the myocardium, indicating regional fatty acid metabolic abnormalities.
  • 血液生化学検査 BNP濃度測定の意義--重症度評価,病態把握,治療効果判定 (心不全(上)最新の基礎・臨床研究の進歩) -- (診断学・検査の進歩)
    蔦本 尚慶, 堀江 稔
    日本臨床 65(0) 417-425 2007年04月
  • 抗アルドステロン薬の有用性
    蔦本 尚慶, 林 優, 石川 千登世, 前田 圭子, 酒井 宏, 大野 慶人, 和田 厚幸, 堀江 稔
    循環制御 25(1) 10-17 2004年03月
  • リモデリングの予防と改善は可能か
    堀江 稔
    日本内科学会雑誌 96 2007年02月
  • かかりつけ医と心不全 慢性心不全の検査 (特集 かかりつけ医が診る心不全)
    蔦本 尚慶, 堀江 稔
    クリニカルプラクティス 26(1) 16-23 2007年01月
  • 薬剤性QT延長症候群 (特集 精神料病院で気をつけるべき身体合併症)
    西尾 由貴子, 堀江 稔
    日本精神科病院協会雑誌 26(7) 681-684 2007年
  • 心筋マーカー
    最新医学 別冊 循環器7 58-67 2007年
  • 慢性心不全の検査
    クリニカルプラクティス 26(1) 16-23 2007年
  • Brugada症候群とLQT3のオーバーラップ:SCN5A変異の臨床的特徴と分子メカニズム
    Jornal of Cardiology 50 132-132 2007年
  • アディポネクチンと心不全予後-BMIによる検討
    Journal of Cardiology 50 337-337 2007年
  • アトルバスタチンは非虚血性心不全患者の心臓交感神経活性を改善する
    Journal of Cardiology 50 431-431 2007年
  • 冠血管機能の性差:冠攣縮性狭心症と胸痛症候群の検討
    Journal of Cardiology 50 137-137 2007年
  • 心筋マーカー
    急性冠症候群 58-67 2007年
  • ANPとBNPを病態診断にいかす
    新心臓病診療プラクチイス 68-72 2007年
  • 冠血管機能の性差:冠攣縮性狭心症と胸痛症候群の検討
    第55回日本心臓病学会学術集会 2007年
  • Brugada症候群とLQT3のオーバーラップ:SCN5A変異の臨床的特徴と分子メカニズム
    第55回日本心臓病学会学術集会 2007年
  • アディポネクチンと心不全予後-BMIによる検討
    第55回日本心臓病学会学術集会 2007年
  • アトルバスタチンは非虚血性心不全患者の心臓交感神経活性を改善する
    第55回日本心臓病学会学術集会 2007年
  • 心不全患者におけるBNPとNT-proBNP分泌動態の比較
    第55回日本心臓病学会学術集会 2007年
  • 高分子アデイポネクチンは心不全予後の指標として有用か?
    第55回 日本心臓病学会学術集会 2007年
  • バイオマカーとしてのナトリウム利尿ペプチド(BNP, N端-proBNP)と腎機能
    最新医学 62(9) 141(1967)-147(1973) 2007年
  • Transcardiac increase in tumor necrosis factor-α and left ventricular end-diastolic volume in patients with dilated cardiomyopathy
    Takayoshi Tsutamoto, Atsuyuki Wada, Masato Ohnishi, Takashi Tsutsui, Chitose Ishii, Keijin Ohno, Masanori Fujii, Takehiro Matsumoto, Takashi Yamamoto, Tomoyuki Takayama, Tomohiro Dohke, Minoru Horie
    European Journal of Heart Failure 6(2) 173-180 2004年03月
    Background: It remains unclear whether tumor necrosis factor (TNF)-α and interleukin-6 (IL-6) are secreted from the failing heart and whether there is a relationship between the transcardiac gradients of these cytokines and left ventricular (LV) remodeling. Aims: This study evaluated the relationship between transcardiac gradients of cytokines and LV volume and function in congestive heart failure patients with dilated cardiomyopathy (DCM). Methods and results: We measured the plasma levels of TNF-α and IL-6 in the aortic root (Ao) and the coronary sinus (CS) in 60 patients with DCM. There was no difference in plasma IL-6 between the Ao and the CS. However, the plasma TNF-α level was significantly higher in the CS than that in the Ao. There was a significant correlation between the transcardiac gradient of plasma TNF-α and the LV end-diastolic volume index (LVEDVI) and LV ejection fraction. According to stepwise multivariate analyses, the transcardiac increase of TNF-α showed an independent and significantly positive relationship with a large LVEDVI. Conclusions: These results indicate that the elevated plasma TNF-α is partly derived from the failing heart in patients with DCM and that TNF-α plays a potential role in structural LV remodeling in patients with DCM. © 2003 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
  • Which heart failure patients would benefit to evaluated plasma adiponectin for predicting mortality risk in Japan.
    第11回日本心不全学会 2007年
  • Angiotensin-converting enzyme insertion/deletion polymorphism modulates coronary release of tissue plasminogen activator in response to bradykinin
    Naoto Ohira, Tetsuya Matsumoto, Shinji Tamaki, Hiroyuki Takashima, Yasuhiro Tarutani, Tetsunobu Yamane, Yo Yasuda, Minoru Horie
    Hypertension Research 27(1) 39-45 2004年01月
    The aim of this study was to assess the relationship between the angiotensin converting enzyme gene (ACE) genotype and endothelium-dependent coronary vasomotor and fibrinolytic activity. The ACE DD genotype has been reported to be a risk factor for myocardial infarction. However, the mechanism is unknown. The fibrinolytic and renin-angiotensin systems are linked via ACE at the vascular beds. We studied 73 patients (II: n=24; ID: n=37; DD: n=12) who underwent diagnostic cardiac catheterization. Graded doses of bradykinin (BK) (0.2, 0.6, 2.0 μg/min) and acetylcholine (30,100 μg/min) were administered into the left coronary artery. Coronary blood flow (CBF) was evaluated by measuring Doppler flow velocity. Blood samples were taken from the aorta (Ao) and the coronary sinus (CS). Coronary release of tPA antigen was determined as a CS-Ao gradient×CBF×[(100-hematocrit) / 100]. ACE genotypes were determined using polymerase chain reaction. The ACE genotype did not appear to affect coronary macro- and microvascular responses induced by BK or acetylcholine. Coronary tissue plasminogen activator (tPA) release induced by BK was depressed in subjects with the ACE DD genotype. ACE levels in the DD genotype were significantly higher than those in the ID or II genotype. In all of the subjects, there was a significant negative correlation between the serum level of ACE activity and net coronary tPA release in response to BK at 0.6 μg/min. In conclusions, the DD genotype of the ACE gene impairs the coronary release of tPA induced by BK.
  • Renin may have an important role in cardio-renal interaction in patients with heart failure
    第11回日本心不全学会 2007年
  • Alpha-adducin gene and hypertension
    Shinji Tamaki, Yasuyuki Nakamura, Minoru Horie, Masahiko Kinoshita, Naoharu Iwai
    Nippon rinsho. Japanese journal of clinical medicine 62 Suppl 3 108-111 2004年01月
  • 心房リモデリングの予防と改善は可能か
    第104回 日本内科学会 2007年
  • Arrhythmias and natriuretic polypeptides
    Minoru Horie
    Nippon rinsho. Japanese journal of clinical medicine 62 Suppl 9 101-102 2004年01月
  • 心房筋リモデリングを考慮したヒト心房細動in silicoモデルにおけるアミオダロンの急性効果と慢性効果
    第12回アミオダロン研究会 2007年
  • Brain natriuretic peptide
    Takayoshi Tsutamoto, Minoru Horie
    Rinsho byori. The Japanese journal of clinical pathology 52 655-668 2004年01月
    Plasma levels of various neurohumoral factors are activated and have an important role of the pathophysiology of congestive heart failure (CHF). Atrial natriuretic peptide (ANP) and brain (or B-type) natriuretic peptide (BNP) are secreted from cardiomyocytes in response to atrial or ventricular wall stretch. The natriuretic peptides have a fundamental role in cardiovascular remodeling, volume homeostasis, and the response to myocardial injury. Clinical investigations of these peptides have focused on their diagnostic usefulness for heart failure and left ventricular dysfunction and their prognostic usefulness after acute coronary syndromes and heart failure. In patients with left ventricular systolic dysfunction, a high plasma BNP level is an independent prognostic predictor of CHF patients, suggesting that the compensatory activity of the cardiac natriuretic peptide system is attenuated as mortality increases in chronic CHF patients with high plasma levels of ANP and BNP. BNP is more useful than ANP for diagnosis and management of CHF. Recently, rapid BNP assay is available in our country, rapid measurement of BNP in the emergency department may improve the evaluation and treatment of patients with acute dyspnea and thereby reduced the time to discharge and the total cost of treatment. In addition, BNP-guided treatment of heart failure may reduce total cardiovascular events, and delayed time to first event combination with intensive clinically guided treatment.
  • ICD埋込を行った特発性心室細動の19歳男性例
    伊藤 誠, 八尾 武憲, 小澤 友哉, 堀江 稔, 杉本 喜久, 八木 崇文, 武田 晋作, 福原 怜, 藤田 真也, 玉井 秀男
    心電図 24(4) 74-74 2004年
  • 第30回 比較心電図研究会:薬剤による心電図変化: 遺伝子異常の関与
    堀江 稔
    心電図 24(1) 64-69 2004年
  • Insulinotropic action of glutamate is dependent on the inhibition of ATP-sensitive potassium channel activities in MIN 6 β cells
    Hidenori Katsuta, Sachihiko Ozawa, Tomonori Ninomiya, Tatsuhiro Shimoyama, Eisuke Ito, Toshiaki Tanaka, Shinya Yamaguchi, Hiroshi Katahira, Shinya Nagamatsu, Minoru Horie, Minoru Horie, Hitoshi Ishida
    Biochemical and Biophysical Research Communications 311(3) 660-664 2003年11月
    To investigate the cellular mechanism of insulinotropic effect of glutamate in pancreatic β cells, we utilized patch-clamp technique to monitor directly the activities of ATP-sensitive potassium channels (K ATP channels). Dimethylglutamate (5mM), a membrane-permeable analog of glutamate, augmented the insulin release induced by the stimulatory concentrations of glucose (p < 0.05-0.01). In the cell-attached configurations, dimethylglutamate reversibly and significantly suppressed the K ATP channel activities (p < 0.01). On the other hand, no significant effect was observed when glutamate itself was applied to the inside-out patches, whereas the prompt and reversible sup pression was recorded in the case of ATP (p < 0.01). These results indicate that the insulinotropic action of glutamate in β cells could be derived from the inhibition of K ATP channel activities, probably due to generation of messengers via intracellular metabolism such as ATP. © 2003 Elsevier Inc. All rights reserved.
  • Proton Magnetic Resonance Spectroscopy can Detect Creatine Depletion Associated with the Progression of Heart Failure in Cardiomyopathy
    Ichiro Nakae, Kenichi Mitsunami, Kenichi Mitsunami, Tomoko Omura, Takahiro Yabe, Takayoshi Tsutamoto, Shinro Matsuo, Masayuki Takahashi, Shigehiro Morikawa, Toshiro Inubushi, Yasuyuki Nakamura, Masahiko Kinoshita, Minoru Horie
    Journal of the American College of Cardiology 42(9) 1587-1593 2003年11月
    OBJECTIVES: This study noninvasively examined total creatine (CR) of the myocardium in dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM) using proton magnetic resonance spectroscopy ( 1 H-MRS). BACKGROUND: Abnormalities in CR metabolism in failing hearts have been reported. A biochemical study suggested that myocardial metabolic changes are very similar in DCM and HCM despite the different heart failure (HF) mechanisms. METHODS: Using cardiac-gated 1 H-MRS with magnetic resonance image (MRI) -guided point-resolved spectroscopy (PRESS) localization, we quantitatively measured septal CR. Patients with either DCM (n = 11) or HCM (n = 7) and age-matched normal subjects (n = 14) were examined. RESULTS: Myocardial CR was significantly lower in DCM patients (16.1 ± 4.5 μmol/g wet weight [range 10.2 to 22.9], p < 0.05) than that in subjects with normal hearts (27.6 ± 4.1 μmol/g [range 21.4 to 36.2]). Myocardial CR in HCM patients (22.6 ± 8.1 μmol/g [range 12.2 to 34.5] ) was significantly lower than that in subjects with normal hearts (p < 0.05) but was significantly higher than that in DCM patients (p < 0.05). In 18 patients with either DCM or HCM, myocardial CR correlated positively with left ventricular ejection fraction (LVEF) (y = 0.22x + 9.8, r = 0.73, p = 0.0006) but correlated negatively with plasma B-type natriuretic peptide (BNP) levels (y = -0.012x + 22.4, r = -0.54, p = 0.022). CONCLUSIONS: This study showed that 1 H-MRS can noninvasively detect CR depletion associated with the severity of HF in cardiomyopathy. © 2003 by the American College of Cardiology Foundation.
  • Genetic background predisposing the drug-induced long QT syndrome
    Minoru Horie
    Folia Pharmacologica Japonica 121(6) 401-407 2003年06月
    Molecular and cellular mechanisms underlying the QT prolongation have been elucidated largely because of the recent understanding of the generation of the congenital forms of QT prolongation; i.e., the long QT syndrome. To date, at least 7 different genes that modulate cardiac ion channels were identitied to be associated with the syndrome. In the clinical setting, the drug-induced long QT syndrome is more frequently seen and therefore important. We found several mutations as well as an SNP specific among the Japanese population in probands referred to as the secondary long QT patients, including the drug-induced cases. These findings raised the potential that there are also predisposing risk factors at patient's side.
  • Immediate administration of mineralocorticoid receptor antagonist spironolactone prevents post-infarct left ventricular remodeling associated with suppression of a marker of myocardial collagen synthesis in patients with first anterior acute myocardial in
    Masaru Hayashi, Takayoshi Tsutamoto, Atsuyuki Wada, Takashi Tsutsui, Chitose Ishii, Keijin Ohno, Masanori Fujii, Atsushi Taniguchi, Tomokazu Hamatani, Yoshitaka Nozato, Ken Kataoka, Naoki Morigami, Masato Ohnishi, Masahiko Kinoshita, Minoru Horie
    Circulation 107(20) 2559-2565 2003年05月
    Background - Aldosterone (ALD) has been shown to stimulate cardiac collagen synthesis and fibroblast proliferation via activation of local mineralocorticoid receptors. In patients with acute myocardial infarction, we demonstrated that ALD was extracted through the infarct heart and extracting ALD-stimulated post-infarct left ventricular (LV) remodeling. Methods and Results - To evaluate the effect of mineralocorticoid receptor antagonist (MRA) spironolactone on post-infarct LV remodeling, 134 patients with first anterior acute myocardial infarction were randomly divided into the MRA (n=65) or non-MRA (n=69) groups after revascularization. All patients were administered angiotensin-converting enzyme (ACE) inhibitor and study drug just after revascularization. Left ventriculography with contrast medium was performed at the acute stage and after 1 month to evaluate LV remodeling. ALD was measured at aortic root and coronary sinus. There was no difference in the baseline characteristics including infarct size and LV performance between the two groups. However, LV ejection fraction was significantly improved in the MRA group compared with that in the non-MRA group (46.0±0.6% to 53.2±0.8% versus 46.5±0.8% to 51.0±0.8%, P interaction =0.012). LV end-diastolic volume index was significantly suppressed in the MRA group compared with that in non-MRA group (86.5±1.0 to 90.6±2.4 versus 87.5±1.3 to 106.8±3.5 mL/m 2 , P interaction =0.002). Transcardiac extraction of ALD through the heart was significantly suppressed in the MRA group (P interaction =0.001), and plasma procollagen type III aminoterminal peptide level, a biochemical marker of fibrosis, was significant lower in the MRA group compared with the non-MRA group (P interaction =0.002). Conclusions - These findings indicate that MRA combined with ACE inhibitor can prevent post-infarct LV remodeling better than ACE inhibitor alone in association with the suppression of a marker of collagen synthesis.
  • 第13回体表心臓微小電位研究会 シンポジウム LQT症候群の病態診断における心電学的アプローチ―VT発生との関連について― 遺伝性QT延長症候群(LQTS)の遺伝子型による心電図学的特徴:LQT1とLQT2における,T波形および再分極指標の運動による変化
    竹中 琴重, 藍 智彦, 小堀 敦志, 二宮 智紀, 大谷 秀夫, 久保田 友之, 堀江 稔, 清水 渉, 高木 洋, 鎌倉 史郎
    心臓 36(1) 32-32 2004年
  • Plasma brain natriuretic peptide as a useful biochemical marker of congestive heart failure
    Takayoshi Tsutamoto, Minoru Horie
    Nippon rinsho. Japanese journal of clinical medicine 61 782-788 2003年01月
    Neurohumoral factors, which is divided to two groups, are activated in patients with congestive heart failure(CHF). One is cardiotoxic biochemical markers such as nor-epinephrine, angiotensin II, endothelin-1, and vasopressin, the other is cardioprotective biochemical markers such as atrial natriuretic peptide, and brain natriuretic peptide (BNP). Among various neurohumoral factors, plasma level of BNP i