Section of Cardiology, Department of Medicine, Rosalind Franklin University of Medicine & Science/The Chicago Medical School, North Chicago, and Mount Sinai Hospital, Chicago, IL, USA.
Am J Ther. 2010 Nov-Dec;17(6):e193-201. doi: 10.1097/MJT.0b013e3181ad3437.
In recent years, there have been considerable advancements in our understanding of the role of ionic channels in mediating cardiac repolarization. Advances in ion channel cloning have generated great interest in the diagnosis and understanding of electrophysiological processes involved in ventricular repolarization, particularly the QT interval prolongation and abnormal T- and T/U-wave morphology associated with torsades de pointes. Unfortunately, a number of drugs are being increasingly recognized to alter the repolarization and, thus, increase the propensity for various cardiac arrhythmias, especially polymorphic ventricular tachycardia, syncope, and even ventricular fibrillation and sudden death. Recently, HIV protease inhibitors have been shown to cause prolongation of ventricular repolarization. This review focuses on electrophysiological mechanisms underlying drug-induced QTc prolongation in relation to protease inhibitors and its clinical implications.
近年来，我们对离子通道在介导心脏复极中的作用有了相当多的了解。离子通道克隆技术的进步极大地激发了人们对诊断和理解涉及心室复极的电生理过程的兴趣，特别是与尖端扭转型室性心动过速相关的 QT 间期延长和异常 T 波和 T/U 波形态。不幸的是，越来越多的药物被认识到会改变复极，从而增加各种心律失常的倾向，特别是多形性室性心动过速、晕厥，甚至心室颤动和猝死。最近，已经表明 HIV 蛋白酶抑制剂会导致心室复极的延长。这篇综述重点介绍了与蛋白酶抑制剂相关的药物引起的 QT c 延长的电生理机制及其临床意义。
