Roden Dan M, Viswanathan Prakash C
Department of Medicine, Oates Institute for Experimental Therapeutics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
J Clin Invest. 2005 Aug;115(8):2025-32. doi: 10.1172/JCI25539.
The QT interval is the electrocardiographic manifestation of ventricular repolarization, is variable under physiologic conditions, and is measurably prolonged by many drugs. Rarely, however, individuals with normal base-line intervals may display exaggerated QT interval prolongation, and the potentially fatal polymorphic ventricular tachycardia torsade de pointes, with drugs or other environmental stressors such as heart block or heart failure. This review summarizes the molecular and cellular mechanisms underlying this acquired or drug-induced form of long QT syndrome, describes approaches to the analysis of a role for DNA variants in the mediation of individual susceptibility, and proposes that these concepts may be generalizable to common acquired arrhythmias.
QT间期是心室复极的心电图表现，在生理条件下具有变异性，并且可被多种药物显著延长。然而，基线间期正常的个体很少会因药物或其他环境应激因素（如心脏传导阻滞或心力衰竭）而出现QT间期过度延长以及潜在致命的多形性室性心动过速——尖端扭转型室速。本综述总结了这种获得性或药物诱导型长QT综合征的分子和细胞机制，描述了分析DNA变异在个体易感性介导中作用的方法，并提出这些概念可能适用于常见的获得性心律失常。
