Abstract：
Amiodarone is a benzofuran-based class III antiarrhythmic agent frequently used for the treatment of atrial and ventricular arrhythmias. The primary target of class III antiarrhythmic drugs is the cardiac human ether-a-go-go-related gene (hERG) encoded channel, KCNH2, commonly known as HERG, that conducts the rapidly activating delayed rectifier potassium current (IKr). Like other class III antiarrhythmic drugs, amiodarone exerts its physiologic effects mainly through IKr blockade, delaying the repolarization phase of the action potential and extending the effective refractory period. However, while many class III antiarrhythmics, including sotalol and dofetilide, can cause long QT syndrome (LQTS) that can progress to torsade de pointes, amiodarone displays less risk of inducing this fatal arrhythmia. This review article discusses the arrhythmogenesis in LQTS from the aspects of the development of early afterdepolarizations (EADs) associated with Ca2+ current, transmural dispersion of repolarization (TDR), as well as reverse use dependence associated with class III antiarrhythmic drugs to highlight electropharmacological effects of amiodarone on the myocardium.
摘要：
胺碘酮是一种基于苯并呋喃的III类抗心律失常药，常用于治疗房性和室性心律失常。III类抗心律失常药物的主要目标是心脏人类ether-a-go-go相关基因（hERG）编码通道，KCNH2，俗称HERG，传导快速激活延迟整流钾电流(IKr)。像其他III类抗心律失常药物一样，胺碘酮主要通过IKr阻滞发挥其生理作用，延缓动作电位的复极化阶段，延长有效不应期。然而,虽然许多III类抗心律失常药，包括索他洛尔和多非利特,可导致长QT综合征（LQTS），可发展为尖端扭转，胺碘酮显示诱发这种致命心律失常的风险较小。本文从与Ca2电流相关的早期后去极化（EADs）的发展方面讨论了LQTS中的心律失常发生，透壁复极色散（TDR），以及与III类抗心律失常药物相关的反向使用依赖，以突出胺碘酮对心肌的电药理作用。
