研究者詳細 - 森田　宏

論文 - 森田　宏

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発熱時にBrugada型心電図を合併したWPW症候群の1例

池田悦子, 武田賢治, 西井伸洋, 永瀬聡, 幡芳樹, 中村一文, 森田宏, 草野研吾, 寒川睦子

Circulation Journal 73 ( Suppl.II ) 968 - 968 2009年4月

慢性活動性EBウイルス感染症に伴う心筋炎を認めた一症例

田中正道, 中村一文, 川合晴朗, 多田毅, 村上正人, 平松茂樹, 西井伸洋, 永瀬聡, 幡芳樹, 森田宏, 草野研吾, 岩月啓氏, 由谷親夫

循環器科 65 ( 2 ) 219 - 219 2009年2月

Fragmented QRS as a marker of conduction abnormality and a predictor of prognosis of Brugada syndrome. 国際誌

Hiroshi Morita, Kengo F Kusano, Daiji Miura, Satoshi Nagase, Kazufumi Nakamura, Shiho T Morita, Tohru Ohe, Douglas P Zipes, Jiashin Wu

Circulation 118 ( 17 ) 1697 - 704 2008年10月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Conduction abnormalities serve as a substrate for ventricular fibrillation (VF) in patients with Brugada syndrome (BS). Signal-averaged electrograms can detect late potentials, but the significance of conduction abnormalities within the QRS complex is still unknown. The latter can present as multiple spikes within the QRS complex (fragmented QRS [f-QRS]). We hypothesized that f-QRS could indicate a substrate for VF and might predict a high risk of VF for patients with BS. METHODS AND RESULTS: In study 1, we analyzed the incidence of f-QRS in 115 patients with BS (13 resuscitated from VF, 28 with syncope, and 74 asymptomatic). f-QRS was observed in 43% of patients, more often in the VF group (incidence of f-QRS: VF 85%, syncope 50%, and asymptomatic 34%, P<0.01). SCN5A mutations occurred more often in patients with f-QRS (33%) than in patients without f-QRS (5%). In patients with syncope or VF, only 6% without f-QRS experienced VF during follow-up (43+/-25 months), but 58% of patients with f-QRS had recurrent syncope due to VF (P<0.01). In study 2, to investigate the mechanism of f-QRS, we studied in vitro models of BS in canine right ventricular tissues (n=4) and optically mapped multisite action potentials. In the experimental model of BS, ST elevation resulted from a large phase 1 notch of the action potential in the epicardium, and local epicardial activation delay reproduced f-QRS in the transmural ECG. CONCLUSIONS: f-QRS appears to be a marker for the substrate for spontaneous VF in BS and predicts patients at high risk of syncope.

DOI： 10.1161/CIRCULATIONAHA.108.770917

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Novel SCN5A Mutations and SNP in Patients with Brugada Syndrome

Kazufumi Nakamura, Daiji Miura, Kaoru Kobayashi, Mamoru Ouchida, Kenji Shimizu, Iori Ohmori, Nobuhiro Nishii, Satoshi Nagase, Hiroshi Morita, Yoshiki Hata, Takefumi Oka, Kengo Kusano, Tohru Ohe

CIRCULATION 118 ( 18 ) S981 - S981 2008年10月

特発性2方向性心室頻拍の臨床電気生理学的機序の検討

杉山洋樹, 森田宏, 三浦大志, 永瀬聡, 中村一文, 岡岳文, 草野研吾, 大江透

心電図 28 ( 5 ) 480 - 480 2008年10月

Brugada症候群患者における心室性不整脈の発生とSCN5A変異の関連

森田宏, 三浦大志, 中村一文, 永瀬聡, 草野研吾, 大江透

心電図 28 ( 5 ) 484 - 484 2008年10月

Brugada症候群におけるICD作動の予測因子

西井伸洋, 森田宏, 平松茂樹, 多田毅, 村上正人, 三浦大志, 永瀬聡, 中村一文, 岡岳文, 大江透, 草野研吾

心電図 28 ( 5 ) 489 - 489 2008年10月

Brugada症候群の病態合併不整脈や遺伝子異常について

草野研吾, 森田宏, 永瀬聡, 中村一文, 大江透

心電図 28 ( 5 ) 418 - 418 2008年10月

Brugada症候群における心電図パラメーターの経時的変化

中川晃志, 西井伸洋, 永瀬聡, 森田宏, 中村一文, 岡岳文, 大江透, 草野研吾

心電図 28 ( 5 ) 485 - 485 2008年10月

ウェーブレット解析によるブルガダ症候群の加算平均心電図の検討

野坂和正, 森田宏, 西井伸洋, 永瀬聡, 中村一文, 岡岳文, 草野研吾, 大江透

心電図 28 ( 5 ) 473 - 473 2008年10月

AED(自動体外式除細動器)の有効性と限界

高谷陽一, 西井伸洋, 永瀬聡, 中村一文, 森田宏, 岡岳文, 草野研吾

心電図 28 ( 5 ) 481 - 481 2008年10月

Abnormal Atrial Electrophysiological Vulnerability and Structural Atrial Remodeling In High-Risk Patients with Brugada Syndrome: Assessment with Electrophysiology and Echocardiography

Norihisa Toh, Hiroshi Morita, Manabu Taniguchi, Nobuhisa Watanabe, Yasuharu Tanabe, Daiji Miura, Satoshi Nagase, Kazufumi Nakamura, Kengo F. Kusano, Tohru Ohe

CIRCULATION 118 ( 18 ) S775 - S775 2008年10月

The QT syndromes: long and short. 国際誌

Hiroshi Morita, Jiashin Wu, Douglas P Zipes

Lancet (London, England) 372 ( 9640 ) 750 - 63 2008年8月

記述言語：英語掲載種別：研究論文（学術雑誌）

This Seminar presents the most recent information about the congenital long and short QT syndromes, emphasising the varied genotype-phenotype association in the ten different long QT syndromes and the five different short QT syndromes. Although uncommon, these syndromes serve as a Rosetta stone for the understanding of inherited ion-channel disorders leading to life-threatening cardiac arrhythmias. Ionic abnormal changes mainly affecting K(+), Na(+), or Ca(2+) currents, which either prolong or shorten ventricular repolarisation, can create a substrate of electrophysiological heterogeneity that predisposes to the development of ventricular tachyarrhythmias and sudden death. The understanding of the genetic basis of the syndromes is hoped to lead to genetic therapy that can restore repolarisation. Presently, symptomatic individuals are generally best treated with an implantable cardioverter defibrillator. Clinicians should be aware of these syndromes and realise that drugs, ischaemia, exercise, and emotions can precipitate sudden death in susceptible individuals.

DOI： 10.1016/S0140-6736(08)61307-0

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多発性肺動静脈瘻の一例

野坂和正, 永瀬聡, 中村一文, 森田宏, 武田賢治, 岡岳文, 草野研吾

日本心臓病学会誌 2 ( Suppl.I ) 514 - 514 2008年8月

右房内に巨大血栓を認めた一例

森あい子, 川田哲史, 永瀬聡, 中村一文, 森田宏, 武田賢治, 岡岳文, 草野研吾, 大江透, 佐野俊二, 豊永慎二

日本心臓病学会誌 2 ( Suppl.I ) 513 - 513 2008年8月

Repolarization heterogeneity in the right ventricular outflow tract: correlation with ventricular arrhythmias in Brugada patients and in an in vitro canine Brugada model. 国際誌

Hiroshi Morita, Douglas P Zipes, Kengo Fukushima-Kusano, Satoshi Nagase, Kazufumi Nakamura, Shiho T Morita, Tohru Ohe, Jiashin Wu

Heart rhythm 5 ( 5 ) 725 - 33 2008年5月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Brugada syndrome (BrS) is characterized by repolarization abnormality with ST-segment elevation in the right ventricular outflow tract (RVOT). OBJECTIVE: Although action potential (AP) heterogeneity is associated with induction of ventricular arrhythmias (VA) in BrS, clinical evidence and its experimental correlations are still absent and are the focus of this study. METHODS: We evaluated repolarization heterogeneity in 15 patients with BrS using body surface mapping and in 8 pairs of isolated canine RVOT and right ventricular anteroinferior (RVAI) preparations having drug-induced BrS using optical mapping. RESULTS: Patients had large J-ST-segment elevation and long QT interval in the RVOT at baseline. Administration of pilsicainide (1 mg/kg) exaggerated J-ST-segment elevation, caused simultaneous long and short QT intervals in the RVOT, and induced polymorphic ventricular tachycardia (VT) and T wave alternans (TWA). Dispersion of QT within the RVOT after pilsicainide was greater in patients that had syncope or ventricular fibrillation than those that did not. Ventricular arrhythmias originated from the RVOT along with local electrocardiogram changes and TWA. Repolarization heterogeneity was much less in areas outside the RVOT. Inducing BrS increased AP heterogeneity (with and without spike-and-dome) within the RVOT epicardium. Phase 2 reentry and TWA originated from the epicardium in 88% and 50% of RVOT preparations, respectively. In contrast, the RVOT endocardium and RVAI had little AP heterogeneity, with neither reentry nor TWA. CONCLUSION: The instability and heterogeneity of repolarization within the epicardium of the RVOT seem to be associated with arrhythmogenesis in both patients and in the in vitro tissue models of BrS.

DOI： 10.1016/j.hrthm.2008.02.028

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精巣摘出によりBrugada型心電図が消失した心筋ナトリウムチャネル遺伝子変異を有する1症例

森田宏, 草野研吾, 永瀬聡, 三浦大志, 中村一文, 大江透

Journal of Arrhythmia 24 ( Suppl. ) 185 - 185 2008年4月