Hiroshi Mabuchi
Kanazawa University
7 Papers
45 Citations
Hiroshi Mabuchi is an academic researcher from Kanazawa University. The author has contributed to research in topics: Hypertrophic cardiomyopathy & Sudden death. The author has an hindex of 7, co-authored 7 publications.
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Papers
T‐peak to T‐end interval may be a better predictor of high‐risk patients with hypertrophic cardiomyopathy associated with a cardiac troponin i mutation than qt dispersion
Shimizu M,Hidekazu Ino,Kazuyasu Okeie,Masato Yamaguchi,Michio Nagata,Kenshi Hayashi,Hideki Itoh,Taku Iwaki,Kotaro Oe,Tetsuo Konno,Hiroshi Mabuchi +10 more
TL;DR: Patients with hypertrophic cardiomyopathy associated with a deletion of lysine 183 (K183del) in the cardiac troponin I (cTnI) gene suffer sudden cardiac death at all ages, but the correlation between QT variables andudden cardiac death in these patients remains uncertain.
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Collagen remodeling and cardiac dysfunction in patients with hypertrophic cardiomyopathy: the significance of type III and VI collagens.
Masaru Kitamura,Shimizu M,Hidekazu Ino,Kazuyasu Okeie,Masato Yamaguchi,Noboru Fujino,Hiroshi Mabuchi,Isao Nakanishi +7 more
TL;DR: The relationship between the extent of myocardial interstitial fibrosis, the percentage of each type of collagen, and cardiac function in patients with hypertrophic cardiomyopathy (HC) has not been established.
81
A Novel Missense Mutation in the SCN5A Gene Associated with Brugada Syndrome Bidirectionally Affecting Blocking Actions of Antiarrhythmic Drugs
TL;DR: A novel Brugada mutation N406S is demonstrated, which is associated with the discordant effects on blocking actions of antiarrhythmic drugs as well as the multiple channel gating defects, and emphasis that an antiarrHythmic drug may exert unpredicted effects in patients with channel mutations.
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Clinical and Electrophysiological Characteristics of Brugada Syndrome Caused by a Missense Mutation in the S5‐Pore Site of SCN5A
TL;DR: Electrophysiological characteristics of the R282H channel are suggested to be closely related to the clinical phenotype of Brugada syndrome and a severe reduction in sodium current density and a mild positive shift of activation curve are suggested.
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Autopsy findings in siblings with hypertrophic cardiomyopathy caused by Arg92Trp mutation in the cardiac troponin T gene showing dilated cardiomyopathy‐like features
Shimizu M,Hidekazu Ino,Masato Yamaguchi,Hidenobu Terai,Katsuharu Uchiyama,Masaru Inoue,Masatoshi Ikeda,Atsuhiro Kawashima,Hiroshi Mabuchi +8 more
TL;DR: A large number of patients with HCM have shown dilated cardiomyopathy (DCM)‐like features, and the relationship between genotype and histologic findings is not well known.
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