Mechanisms underlying spontaneous and induced ventricular arrhythmias in patients with idiopathic dilated cardiomyopathy
Mechanisms underlying spontaneous and induced ventricular arrhythmias in patients with idiopathic dilated cardiomyopathy
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DOI：
10.1161/01.cir.98.22.2404
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发表时间：
1998-12-01
期刊：
影响因子：
37.8
通讯作者：
Cain, ME
中科院分区：
文献类型：
--
作者：
Pogwizd, SM;McKenzie, JP;Cain, ME
背景-为了明确与非缺血性心肌病相关的可诱导和自发性室性心律失常的电生理机制，对6例接受心脏移植的特发性扩张型心肌病患者进行了156个壁内部位的三维术中标测，方法和结果：电极密度足以确定74次非持续性室性心动过速中52次的机制（VT）和9例自发性室性心律失常。第一、第二和第三次额外刺激（S-2至S-4）的传导延迟程度逐渐增大（总激活时间[TA]分别为144+/-5，166+/-5和194+/-5 ms），原因是传导缓慢，偶尔出现壁内阻滞。诱发性室性心动过速的第一次搏动来自心内膜下或心外膜下部位，这些部位远离明显传导延迟的区域，这是基于在最后一次额外刺激终止和室性心动过速开始之间没有干预性电活动（123+/-31 ms）的局灶性机制。随后的心搏由局灶性机制引起，TA为127+/-6 ms（P = NS vs VT起始心搏[118+/-5 ms]）。自发性室性心律失常由局灶性机制在心内膜下引发，TA为138+/-5 ms。组织分析表明局灶性激活部位存在不同程度的间质纤维化。传导延迟或阻滞的部位通常表现出显着的间质和/或替代纤维化，但在空间上远离起始VT的部位。结论自发性和诱导性室性心律失常的终末期特发性心肌病患者可以出现在心内膜下或心外膜下的局灶性机制。
Background-To define the electrophysiological mechanism(s) of inducible and spontaneously occurring ventricular arrhythmias associated with nonischemic cardiomyopathy, 3-dimensional intraoperative mapping from 156 intramural sites was performed in 6 patients with idiopathic dilated cardiomyopathy undergoing cardiac transplantation.Methods and Results-Electrode density was sufficient to determine the mechanism for 52 of 74 beats of nonsustained ventricular tachycardia (VT) induced by programmed stimulation and 9 of II bears of spontaneous ventricular arrhythmias. The first, second, and third extrastimuli (S-2 through S-4) conducted with progressively greater degrees of conduction delay (total activation times [TAs] of 144+/-5, 166+/-5, and 194+/-5 ms, respectively) owing to slow conduction and on occasion intramural block. The first beats of induced VT arose from subendocardial or subepicardial sites distant from areas of marked conduction delay by a focal mechanism on the basis of the absence of intervening electrical activity between the termination of the last extrastimulus and the initiation of VT (123+/-31 ms). Subsequent beats arose by a focal mechanism and conducted with a TA of 127+/-6 ms (P = NS versus initiating beats of VT [118+/-5 ms]). Spontaneous ventricular arrhythmias initiated in the subendocardium by a focal mechanism and conducted with a TA of 138+/-5 ms. Tissue analysis demonstrated a variable degree of interstitial fibrosis at sites of focal activation. Sites of conduction delay or block typically exhibited marked interstitial and/or replacement fibrosis but were spatially distant from sites initiating VT.Conclusions-Spontaneous and induced ventricular arrhythmias in patients with end-stage idiopathic cardiomyopathy can arise in the subendocardium or subepicardium by a focal mechanism.