Ventricular hypertrophy amplifies transmural repolarization dispersion and induces early afterdepolarization
Ventricular hypertrophy amplifies transmural repolarization dispersion and induces early afterdepolarization
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DOI：
10.1152/ajpheart.2001.281.5.h1968
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发表时间：
2001-11-01
影响因子：
4.8
通讯作者：
Kowey, PR
中科院分区：
文献类型：
--
作者：
Yan, GX;Rials, SJ;Kowey, PR
采用兔心室楔形标本，观察了左心室肥厚（LVH）对2相早期后除极（EAD）和跨室壁复极离散度（TDR）的影响。同时记录心外膜、心内膜下和心内膜的跨膜动作电位以及跨壁ECG。还绘制了心房肌动作电位时程（APD）。左室肥厚（LVH）使心室APD和QT间期显著延长。内膜下和内膜下APD优先延长与TDR显著增加相关。在不使用APD延长剂的情况下，所有LVH家兔（15/15）在2，000 - 4，000 ms的基本周期长度下，从心内膜下或心内膜下产生2相埃兹。2相EAD可产生“T上R”期外收缩，引发多形性室性心动过速（VT）。本研究提供了来自细胞内记录的第一个直接证据，即在不存在APD延长剂的情况下，可以从兔完整的肥厚LV壁产生2相EAD，导致T上R期外收缩能够在增强的TDR下启动多态性VT。
The effects of left ventricular hypertrophy (LVH) on the generation of phase 2 early afterdepolarization (EAD) and transmural dispersion of repolarization (TDR) were assessed using arterially perfused rabbit ventricular wedge preparations. Transmembrane action potentials from epicardium, subendocardium, and endocardium were simultaneously recorded together with a transmural ECG. Transmural action potential duration (APD) was also mapped. LVH (renovascular hypertension model) produced significant prolongation in ventricular APD and QT interval. Preferential APD prolongation in subendocardium and endocardium was associated with a marked increase in TDR. Phase 2 EADs were generated from subendocardium or endocardium in all LVH rabbits (15 of 15) in the absence of APD prolonging agents at basic cycle lengths of 2,000-4,000 ms. Phase 2 EAD could produce "R on T" extrasystoles, initiating polymorphic ventricular tachycardia (VT). This study provides the first direct evidence from intracellular recordings that phase 2 EAD could be generated from rabbit intact hypertrophied LV wall in the absence of APD prolonging agents, resulting in R on T extrasystoles capable of initiating polymorphic VT under enhanced TDR.