Remodeled left ventricular myocardium remote to infarction sites is the arrhythmogenic substrate for sudden cardiac death

被引:13
作者
Tsai, Chin-Feng [1 ]
Ueng, Kwo-Chang
Wu, Der-Jinn
Tsai, Tsung-Po [2 ]
Lin, Chung-Sheng
机构
[1] Chung Shan Med Univ Hosp, Div Cardiol, Dept Internal Med, Sch Med, Taichung 402, Taiwan
[2] Chung Shan Med Univ Hosp, Dept Surg, Taichung 402, Taiwan
关键词
CLINICAL-IMPLICATIONS; EJECTION FRACTION; VIABLE MYOCARDIUM; CANINE MODEL; DE-POINTES; HYPERTROPHY; SUSCEPTIBILITY; REPOLARIZATION; TACHYCARDIA; FIBRILLATION;
D O I
10.1016/j.mehy.2010.03.036
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
100103 [病原生物学]; 100218 [急诊医学];
摘要
Ventricular tachyarrhythmias are life threatening cardiac arrhythmias and are the most common causes of sudden cardiac death. Greater post-infarction left ventricular remodeling has been shown to have a greater preponderance of ventricular arrhythmias. The hypothesis herein is that adverse structural and electrophysiological remodeling at non-infarcted regions after myocardial infarction constitutes the arrhythmogenic substrate responsible for clinically occurring ventricular arrhythmias leading to sudden cardiac death. Post-infarction patients with more severe left ventricular remodeling (regional hypertrophy) at sites remote to infarction scar might have the highest risk for sudden cardiac death due to lethal ventricular arrhythmias. In the hypertrophic non-infarcted zone, larger action potential duration and repolarization heterogeneity is not in self arrhythmogenic, but can predispose towards arrhythmia development under certain condition, such as transient myocardial ischemia. We should draw more attention to apparently "normal" non-infarction region for further understanding the mechanism of sudden cardiac death. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:368 / 371
页数:4
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