Sartiani Laura, Stillitano Francesca, Cerbai Elisabetta, Mugelli Alessandro
Centro Interuniversitario di Medicina Molecolare e Biofisica Applicata (C.I.M.M.B.A.), Università degli Studi di Firenze, Viale Pieraccini 6, Firenze 50139, Italy.
Can J Physiol Pharmacol. 2009 Feb;87(2):84-90. doi: 10.1139/Y08-109.
Heart failure is a common clinical syndrome occurring as a result of cardiac overload, injury, and a complex interplay among genetic, neurohormonal, inflammatory, and biochemical factors. Occurrence of arrhythmias in heart failure is largely a consequence of disease-induced electrical remodeling of cardiac myocytes, a phenomenon consisting of alterations of ion channels and the ion-transport function that predispose patients to develop lethal arrhythmias. In most cases, the mechanism is the rapid onset of a ventricular tachyarrhythmia progressing to ventricular fibrillation and hemodynamic compromise. This paper highlights some of the important changes in ion channel expression and function that underlie electrical remodeling of the failing heart. Particular attention will be focused on the presence, features, and pharmacologic modulation of f channels expressed in ventricular cardiac myocytes.
心力衰竭是一种常见的临床综合征，由心脏负荷过重、损伤以及遗传、神经激素、炎症和生化因素之间复杂的相互作用引起。心力衰竭时心律失常的发生很大程度上是疾病诱导心肌细胞电重构的结果，这种现象包括离子通道和离子转运功能的改变，使患者易发生致命性心律失常。在大多数情况下，机制是室性快速性心律失常迅速发作，进展为心室颤动和血流动力学障碍。本文重点介绍了衰竭心脏电重构基础的离子通道表达和功能的一些重要变化。将特别关注心室心肌细胞中表达的f通道的存在、特征和药理调节。
