瞬时外向钾电流及通道异常致心力衰竭心律失常的研究进展  

Progress in arrhythmia in heart failure caused by transient outward potassium current and channel abnormalities

作　　者：汪艳丽[1] 李泱[2] 刘金凤[1] 关宣可 常兴 刘如秀[1] WANG Yan-Li;LI Yang;LIU Jin-Feng;GUAN Xuan-Ke;CHANG Xing;LIU Ru-Xiu(Department of Cardiology,Guang′anmen Hospital,China Academy of Chinese Medical Sciences,Beijing 100053,China;Institute of Geriatric Cardiology,Chinese PLA General Hospital,Beijing 100085,China)

机构地区：[1]中国中医科学院广安门医院心血管科,北京100053 [2]中国人民解放军总医院老年心血管病研究所,北京100853

出　　处：《中华老年多器官疾病杂志》2021年第11期859-861,共3页Chinese Journal of Multiple Organ Diseases in the Elderly

基　　金：国家自然科学基金(81904045),北京市自然科学基金(7204297);中国中医科学院优秀青年科技人才专项(ZZ14-YQ-014)。

摘　　要：慢性心力衰竭恶性心律失常发病率、致死率高,严重影响心力衰竭患者生活质量。心肌细胞离子通道异常导致动作电位时程(APD)延长,进而诱发异常触发活动是心力衰竭心律失常发生的主要机制。瞬时外向钾电流(I to)主要参与心肌细胞动作电位(AP)的1期复极,对心力衰竭时APD延长具有重要作用;钾通道相互作用蛋白2(KChIP 2)是I to通道上的的重要功能亚单位,对I to具有关键性调控作用,KChIP 2基因敲除大鼠心肌细胞I to几乎完全消失,心律失常易感性显著增加。本文对慢性心力衰竭心律失常的钾离子通道机制研究进展进行综述,以期为心力衰竭心律失常的治疗靶点提供思路。Chronic heart failure(CHF)has a high incidence rate and mortality rate,seriously affecting the quality of life of patients with heart failure.Prolonged action potential duration(APD)resulting from abnormal ion channels and consequent abnormal triggering activity constitutes the main mechanism of arrhythmia in heart failure.Transient outward potassium current(I to)is mainly involved in the repolarization of AP in cardiomyocytes and plays an important role in prolonging APD in heart failure.Potassium channel interacting protein 2(KChIP 2)is an important functional subunit of I to channel and plays a key role in regulating I to.I to almost completely disappears in cardiomyocytes in KChIP 2-knockout rats,and the susceptibility to arrhythmia increases significantly.This article reviews the progress in potassium channel mechanism of arrhythmia in chronic heart failure with a view to providing new pathways for the treatment targets of arrhythmia in heart failure.

关 键 词：心力衰竭 钾通道相互作用蛋白2 瞬时外向钾电流 心律失常 

分 类 号：R541[医药卫生—心血管疾病]