El-Sherif N, Chinushi M, Caref E B, Restivo M
Department of Medicine, State University of New York Health Science Center and Veterans Affairs Medical Center, Brooklyn 11203, USA.
Circulation. 1997 Dec 16;96(12):4392-9. doi: 10.1161/01.cir.96.12.4392.
The long-QT syndrome (LQTS) is an electrophysiological (EP) entity characterized by prolongation of cardiac repolarization and the occurrence of polymorphic ventricular tachyarrhythmias (VTs), sometimes with a twisting QRS morphology, better known as torsade de pointes (TdP). In the present study, detailed analysis of ventricular tridimensional activation patterns during nonsustained TdP VT was performed to provide an EP mechanism of the periodic transition in QRS axis.
The studies were conducted with the anthopleurin-A canine model of LQTS. Tridimensional isochronal maps of ventricular activation were constructed from 256 bipolar electrograms obtained from the use of 64 plunge needle electrodes. In 26 episodes of nonsustained TdP VT, detailed activation maps could be accurately constructed during QRS-axis transitions in surface ECGs. The initial beat of all VTs consistently arose as a subendocardial focal activity, whereas subsequent beats were due to reentrant excitation in the form of rotating scrolls. The VT ended when reentrant excitation was terminated. In 22 of 26 episodes, the transition in QRS axis coincided with the transient bifurcation of a predominantly single rotating scroll into two simultaneous scrolls involving both the right ventricle and left ventricle separately. The common mechanism for initiation or termination of bifurcation was the development of functional conduction block between the anterior or posterior right ventricle free wall and the ventricular septum. In 4 of 26 episodes, a fast polymorphic VT, with an apparent shift in QRS axis, was due to a predominantly single localized circuit that varied its location and orientation from beat to beat, with the majority of ventricular myocardium being activated in a centrifugal pattern.
The study provides for the first time an EP mechanism for the characteristic periodic transition of the QRS axis during TdP VT in the LQTS.
长QT综合征(LQTS)是一种电生理(EP)疾病,其特征为心脏复极延长及多形性室性心律失常(VTs)的发生,有时伴有QRS波形态扭转,即更熟知的尖端扭转型室速(TdP)。在本研究中,对非持续性TdP室速期间的心室三维激动模式进行了详细分析,以提供QRS轴周期性转变的EP机制。
研究采用LQTS的海葵毒素A犬模型进行。利用64根穿刺针电极获取256个双极电图,构建心室激动的三维等时图。在26次非持续性TdP室速发作中,可在体表心电图QRS轴转变期间准确构建详细的激动图。所有室速的起始搏动均一致地起源于心内膜下局灶性活动,而随后的搏动则是由旋转波形式的折返激动所致。当折返激动终止时,室速结束。在26次发作中的22次,QRS轴的转变与一个主要为单一旋转波瞬时分叉为两个同时存在的分别涉及右心室和左心室的波相关。分叉起始或终止的共同机制是右心室前壁或后壁游离壁与室间隔之间功能性传导阻滞的发生。在26次发作中的4次,一种伴有QRS轴明显偏移的快速多形性室速是由一个主要为单一局部环路所致,该环路逐搏改变其位置和方向,大部分心室心肌以离心方式被激动。
本研究首次为LQTS中TdP室速期间QRS轴的特征性周期性转变提供了EP机制。