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心肌梗死后期折返性室性心动过速的自发终止:犬实验研究

Spontaneous termination of reentry ventricular tachycardia in the late myocardial infarction period: an experimental study in the dog.

作者信息

Ogawa S, Kaplinsky E, Dreifus L S

出版信息

Pacing Clin Electrophysiol. 1979 May;2(3):267-81. doi: 10.1111/j.1540-8159.1979.tb03646.x.

DOI:10.1111/j.1540-8159.1979.tb03646.x
PMID:95291
Abstract

Forty episodes of induced ventricular tachycardia in the late myocardial infarction period (4-6 days old) were analyzed in 12 dogs in an attempt to identify the possible mechanisms for the termination of reentry tachycardia. Multiple epicardial and endocardial composite electrograms were recorded in and around the central ischemic zone of the infarction. During tachycardia, the earliest site of activation was identified in the epicardial surface of the border or normal zone immediately adjacent to the ischemic zone in 36 of the 40 episodes, suggesting efferent epicardial spread from the site of the activity. In four instances, the efferent pathways were directed to the endocardial surface. Four distinct patterns of activation sequences were observed during spontaneous termination: (a) a shift of the efferent pathways from epicardial to endocardial site (19 instances); (b) a change of the efferent pathways within the endocardium (4 instances); (c) a shift of the earliest site of activation between the left and right ventricles (9 instances); and (d) no apparent change in the epicardial efferent pathways (4 instances). In four other instances, ventricular tachycardia deteriorated into ventricular fibrillation. In patterns (a) and (c), a shift of the efferent pathways resulted in a more rapid and homogeneous activation of the border and normal zone epicardium. These changes were associated with cessation of delayed or continuous activity in the ischemic zone epicardium, resulting in termination of tachycardia.

摘要

对12只犬在心肌梗死后期(4 - 6日龄)诱发的40次室性心动过速发作进行了分析,以试图确定折返性心动过速终止的可能机制。在梗死中央缺血区及其周围记录了多个心外膜和心内膜复合电图。在心动过速期间,40次发作中有36次最早激动部位位于紧邻缺血区的边界或正常区的心外膜表面,提示激动从该部位向外膜传出。在4例中,传出途径指向心内膜表面。在自发终止期间观察到4种不同的激动顺序模式:(a)传出途径从心外膜部位转移到心内膜部位(19例);(b)心内膜内传出途径的改变(4例);(c)最早激动部位在左、右心室之间转移(9例);以及(d)心外膜传出途径无明显变化(4例)。在另外4例中,室性心动过速恶化为心室颤动。在模式(a)和(c)中,传出途径的转移导致边界和正常区心外膜更快且更均匀的激动。这些变化与缺血区心外膜延迟或持续活动的停止相关,从而导致心动过速终止。

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