Akar Fadi G, Tomaselli Gordon F
Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Ann Med. 2005;37(1):44-54. doi: 10.1080/07853890510007214.
Electrophysiological remodeling in heart failure (HF) is characterized by major changes in ion channel function and expression that alter the electrical phenotype and predispose to the development of lethal ventricular tachyarrhythmias. In this article, we provide a review of our current understanding of HF-induced ion channel dysfunction by highlighting changes in potassium and sodium currents, pumps, and exchangers as well as calcium handling proteins. We further relate these changes in ion channel function to abnormalities in impulse generation, conduction, and repolarization with a view towards identifying potentially novel targets for anti-arrhythmic therapy for this public health epidemic.
心力衰竭（HF）中的电生理重塑的特征是离子通道功能和表达发生重大变化，这些变化改变了电生理表型，并易引发致命性室性心律失常。在本文中，我们通过重点介绍钾离子和钠离子电流、泵、交换体以及钙处理蛋白的变化，对目前我们对HF诱导的离子通道功能障碍的理解进行综述。我们还将离子通道功能的这些变化与冲动产生、传导和复极化异常联系起来，以期为这种公共卫生流行病确定抗心律失常治疗的潜在新靶点。
