儿茶酚胺能多态性室性心动过速
Brugada综合征
医学
短QT综合征
内科学
心脏病学
长QT综合征
心室颤动
室性心动过速
纤颤
心房颤动
QT间期
兰尼碱受体2
兰尼定受体
钙
作者
Arthur A.M. Wilde,Hasan Garan,Penelope A. Boyden
出处
期刊:Heart Rhythm
[Elsevier]
日期:2019-07-01
卷期号:16 (7): 1121-1126
被引量:27
标识
DOI:10.1016/j.hrthm.2019.01.034
摘要
Much has been written about arrhythmias in structurally normal hearts. In this review, we focus on rapid ventricular arrhythmias that occur in hearts having a pathogenic genetic variant that has been found in families in which arrhythmias occur. We discuss these mutations in terms of their effect on cardiac cell electrical function and initiation of arrhythmias. We also focus on Purkinje cells, their anatomic networks, and their molecular signatures as the sites of origin of arrhythmias. We discuss therapeutic options for treatment of these potentially life-threatening arrhythmias. Although all Purkinje-based arrhythmias are not included (eg, conduction block rhythms), syndromes discussed include idiopathic ventricular fibrillation, catecholaminergic polymorphic ventricular tachycardia, long QT syndrome, Andersen-Tawil syndrome, and Brugada syndrome. Much has been written about arrhythmias in structurally normal hearts. In this review, we focus on rapid ventricular arrhythmias that occur in hearts having a pathogenic genetic variant that has been found in families in which arrhythmias occur. We discuss these mutations in terms of their effect on cardiac cell electrical function and initiation of arrhythmias. We also focus on Purkinje cells, their anatomic networks, and their molecular signatures as the sites of origin of arrhythmias. We discuss therapeutic options for treatment of these potentially life-threatening arrhythmias. Although all Purkinje-based arrhythmias are not included (eg, conduction block rhythms), syndromes discussed include idiopathic ventricular fibrillation, catecholaminergic polymorphic ventricular tachycardia, long QT syndrome, Andersen-Tawil syndrome, and Brugada syndrome.
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