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致心律失常性右室心肌病是右束支传导阻滞、ST段抬高和猝死综合征的基础。

Arrhythmogenic right ventricular cardiomyopathy underlies syndrome of right bundle branch block, ST-segment elevation, and sudden death.

作者信息

Tada H, Aihara N, Ohe T, Yutani C, Hamada S, Miyanuma H, Takamiya M, Kamakura S

机构信息

Division of Cardiology, National Cardiovascular Center, Osaka, Japan.

出版信息

Am J Cardiol. 1998 Feb 15;81(4):519-22. doi: 10.1016/s0002-9149(97)00942-9.

DOI:10.1016/s0002-9149(97)00942-9
PMID:9485151
Abstract

Right ventricular morphologic and/or histologic abnormalities were present in 5 of 6 Japanese men with the Brugada syndrome. Results indicate that arrhythmogenic right ventricular cardiomyopathy may underlie the cardiac manifestations in the Brugada syndrome.

摘要

6名患有Brugada综合征的日本男性中有5人存在右心室形态学和/或组织学异常。结果表明，致心律失常性右心室心肌病可能是Brugada综合征心脏表现的潜在原因。

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引用本文的文献

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Arrhythmogenic right ventricular cardiomyopathy mimicking Brugada - a case report.酷似Brugada综合征的致心律失常性右室心肌病——一例报告
Ann Med Surg (Lond). 2023 Aug 15;85(10):5035-5038. doi: 10.1097/MS9.0000000000000933. eCollection 2023 Oct.
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Genetic and Molecular Mechanisms in Brugada Syndrome.Brugada 综合征的遗传和分子机制。
Cells. 2023 Jul 5;12(13):1791. doi: 10.3390/cells12131791.
3
Mechanisms of Arrhythmias in the Brugada Syndrome. Brugada 综合征中的心律失常机制。
Int J Mol Sci. 2020 Sep 25;21(19):7051. doi: 10.3390/ijms21197051.
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Relationship Between Arrhythmogenic Right Ventricular Cardiomyopathy and Brugada Syndrome: New Insights From Molecular Biology and Clinical Implications.致心律失常性右室心肌病与Brugada综合征的关系：分子生物学新见解及临床意义
Circ Arrhythm Electrophysiol. 2016 Apr;9(4):e003631. doi: 10.1161/CIRCEP.115.003631.
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An overlap of Brugada syndrome and arrhythmogenic right ventricular cardiomyopathy/dysplasia.布加综合征与致心律失常性右室心肌病/发育异常的重叠。
J Arrhythm. 2016 Feb;32(1):70-3. doi: 10.1016/j.joa.2015.10.007. Epub 2015 Nov 30.
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Basis for the Induction of Tissue-Level Phase-2 Reentry as a Repolarization Disorder in the Brugada Syndrome.Brugada综合征中作为复极障碍的组织水平2期折返诱导的基础。
Biomed Res Int. 2015;2015:197586. doi: 10.1155/2015/197586. Epub 2015 Oct 25.
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Arrhythmic substrate, slowed propagation and increased dispersion in conduction direction in the right ventricular outflow tract of murine Scn5a+/- hearts.在小鼠Scn5a+/-心脏的右心室流出道中，心律失常基质、传导减慢以及传导方向上的离散度增加。
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