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Mechanisms underlying arrhythmogenesis in long QT syndrome
Lankipalli, RS; Zhu, TG; Guo, DL; Yan, GX
关键词Long Qt Syndrome Arrhythmogenesis TorsaDes De Pointes
刊名JOURNAL OF ELECTROCARDIOLOGY
2005-10-01
DOI10.1016/j.jelectrocard.2005.06.008
suppl.S期:4页:69-73
收录类别SCI ; ISTP
文章类型Proceedings Paper
WOS标题词Science & Technology
类目[WOS]Cardiac & Cardiovascular Systems
研究领域[WOS]Cardiovascular System & Cardiology
关键词[WOS]TORSADE-DE-POINTES ; LEFT-VENTRICULAR WALL ; TRANSMURAL DISPERSION ; CELLULAR BASIS ; M-CELLS ; T-WAVE ; EARLY AFTERDEPOLARIZATION ; REPOLARIZATION ; INTERVAL ; ARRHYTHMIAS
英文摘要

Long QT syndrome is a disease of delayed ventricular repolarization. It manifests clinically as recurrent syncope and sudden cardiac death caused by an atypical form of polymorphic ventricular tachycardia known as torsades de pointes (TdP). Evidence obtained from the studies using the rabbit left and right ventricular wedge preparations indicates that the development of UP is relying not only on the genesis of air R-on-T trigger, but also on the formation of a functional reentrant substrate. When ventricular endocardial or subendocardial repolarization is prolonged either because of gene mutations or by drugs that reduce the net repolarization current, cell membrane potential fluctuates during phase 2 of the action potential phase 2 because of reactivation of L-type calcium Current, that is, the appearance of phase 2 early afterdepolarization (EAD). In the rabbit left ventricular wedge, QT prolongation and EAD due to pure I-Kr inhibition are accompanied by a disproportional increase in transmural dispersion of repolarization (TDR). Early afterdepolarization in endocardium or subendocardium is able to produce new action potentials in cells with a relatively short action potential duration (eg, ventricular epicardium) probably via an electrotonic effect Mien TDR is large enough. This, in turn, results in an R-on-T extrasystole that is capable of initiating UP. Enhanced TDR is essential not only for the genesis of the first initiating beat of TdP by facilitating the propagation of EAD, but also for the maintenance of TdP by serving as a functional reentrant substrate. (c) 2005 Elsevier Inc. All rights reserved.

语种英语
WOS记录号WOS:000233191000014
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被引频次:38[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56648
专题北京大学第二临床医学院_心血管内科
作者单位1.Main Line Hlth Heart Ctr, Wynnewood, PA 19096 USA
2.Lankenau Inst Med Res, Wynnewood, PA 19096 USA
3.Peking Univ, Peoples Hosp, Dept Cardiol, Beijing 100044, Peoples R China
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Lankipalli, RS,Zhu, TG,Guo, DL,et al. Mechanisms underlying arrhythmogenesis in long QT syndrome[J]. JOURNAL OF ELECTROCARDIOLOGY,2005,suppl.S(4):69-73.
APA Lankipalli, RS,Zhu, TG,Guo, DL,&Yan, GX.(2005).Mechanisms underlying arrhythmogenesis in long QT syndrome.JOURNAL OF ELECTROCARDIOLOGY,suppl.S(4),69-73.
MLA Lankipalli, RS,et al."Mechanisms underlying arrhythmogenesis in long QT syndrome".JOURNAL OF ELECTROCARDIOLOGY suppl.S.4(2005):69-73.
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