Janse M J
Department of Clinical, University of Amsterdam, The Netherlands.
Arch Mal Coeur Vaiss. 1999 Apr;92 Spec No 1:9-16.
In this review, a brief overview of the different arrhythmogenic mechanisms is given, emphasizing that the mechanisms for initiation and maintenance of tachyarrhythmias are often not the same. Normal automaticity in Purkinje fibers, surrounded by partially depolarized tissue providing entrance block, is most likely responsible for ventricular premature beats and enhanced automaticity can lead to (rare) cathecholamine dependent ventricular tachycardias. Abnormal automaticity in partially depolarized cells may underlie ectopic atrial tachycardias and accelerated idioventricular rhythms in the subacute phase of myocardial infarction. Triggered activity based on early afterdepolarizations may trigger torsade de pointes in both the congenital and acquired long QT syndrome. The various mutations, affecting both potassium and sodium channels, will be discussed. Cellular calcium overload, which may occur in digitalis intoxication, hypertrophy and heart failure, is the cause for delayed afterdepolarizations and triggered activity. Reentry, anatomical and functional, ordered or reentry, is by far the most common cause of both atrial and ventricular tachycardias and fibrillation. Special attention will be given to the phenomenon of "electrical remodeling" in which prolonged episodes of rapid electrical activity leads to changes in ion channel function, which in their turn cause long lasting electrophysiological alterations.
在本综述中，我们简要概述了不同的致心律失常机制，强调快速性心律失常的起始和维持机制通常并不相同。浦肯野纤维的正常自律性，周围存在部分去极化组织提供传入阻滞，很可能是室性早搏的原因，而自律性增强可导致（罕见的）儿茶酚胺依赖性室性心动过速。部分去极化细胞的异常自律性可能是心肌梗死亚急性期异位房性心动过速和加速性室性自主心律的基础。基于早期后除极的触发活动可能在先天性和获得性长QT综合征中引发尖端扭转型室速。将讨论影响钾通道和钠通道的各种突变。细胞钙超载，可发生在洋地黄中毒、心肌肥厚和心力衰竭时，是延迟后除极和触发活动的原因。折返，包括解剖性和功能性、有序或无序折返，是迄今为止房性和室性心动过速及颤动最常见的原因。将特别关注“电重构”现象，即长时间的快速电活动发作导致离子通道功能改变，进而引起持久的电生理改变。
