Molecular genetic basis of sudden cardiac death

被引：37

作者：

Towbin, JA

机构：

[1] Texas Childrens Hosp, Dept Pediat Cardiol, Houston, TX 77030 USA

[2] Texas Childrens Hosp, Dept Cardiovasc Sci, Houston, TX 77030 USA

[3] Texas Childrens Hosp, Dept Mol & Human Genet, Houston, TX 77030 USA

[4] Baylor Coll Med, Dept Pediat Cardiol, Houston, TX 77030 USA

[5] Baylor Coll Med, Dept Cardiovasc Sci, Houston, TX 77030 USA

[6] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA

来源：

CARDIOVASCULAR PATHOLOGY | 2001年 / 10卷 / 06期

关键词：

long QT syndrome; Brugada syndrome; idiopathic ventricular fibrillation; ion channels; sodium channel; potassium channel; ARVD; arrhythmogenic right ventricular dysplasia; HCM; hypertrophic cardiomyopathy; sarcomere;

D O I：

10.1016/S1054-8807(01)00090-4

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

In this review, the up-to-date understanding of the molecular basis of disorders causing sudden death will be described. Two arrhythmic disorders causing sudden death have recently been well described at the molecular level, the long QT syndromes (LQTS) and Brugada syndrome, and in this article we will review the current scientific knowledge of each disease. A third disorder, hypertrophic cardiomyopathy (HCM), a myocardial disorder causing sudden death, has also been well studied. Finally, a disorder in which both myocardial abnormalities and rhythm abnormalities coexist, arrhythmogenic right ventricular dysplasia (ARVD) will also be described. The role of the pathologist in these studies will be highlighted. (C) 2001 Elsevier Science Inc. All rights reserved.

引用

页码：283 / 295

页数：13

共 137 条

[41] PHOSPHORYLATION SWITCHES SPECIFIC FOR THE CARDIAC ISOFORM OF MYOSIN BINDING PROTEIN-C - A MODULATOR OF CARDIAC CONTRACTION [J].