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犬梗死模型中折返性室性心动过速期间QRS形态自发改变的机制,有时类似于尖端扭转型室速。

Mechanisms for spontaneous changes in QRS morphology sometimes resembling torsades de pointes during reentrant ventricular tachycardia in a canine infarct model.

作者信息

Schmitt H, Cabo C, Costeas C, Coromilas J, Wit A L

机构信息

Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA.

出版信息

J Cardiovasc Electrophysiol. 2001 Jun;12(6):686-94. doi: 10.1046/j.1540-8167.2001.00686.x.

DOI:10.1046/j.1540-8167.2001.00686.x
PMID:11405403
Abstract

INTRODUCTION

Spontaneous changes in QRS morphology during sustained reentrant ventricular tachycardia, occurring gradually or abruptly, causing the tachycardia to be polymorphic, have been described in clinical cases. The purpose of this study was to determine the mechanism for such changes in a canine infarct model.

METHODS AND RESULTS

Reentrant circuits were mapped in the epicardial border zone during sustained ventricular tachycardia in the canine heart, 4 days after left anterior descending coronary occlusion. In 10 tachycardias, there was either an abrupt change in QRS morphology or a gradual change that took up to 25 cycles. When the latter occurred, the ECG resembled torsades de pointes. Maps showed that the predominant mechanism for the change in QRS was a shift in the exit route by which the impulse left the reentrant circuit to activate the ventricles (9/10 tachycardias). Such shifts resulted from small changes in conduction velocity in segments of the circuit, either speeding or slowing, which modified the length of the functional lines of block. Movement of the circuit to a different region was responsible for the change in QRS in only one of these experiments, in which the reentrant mechanism also changed from functional to anatomic.

CONCLUSION

Subtle changes in conduction in reentrant circuits can alter QRS morphology. Changes in the exit route from a stable reentrant circuit can cause the ECG characteristics to resemble torsades de pointes.

摘要

引言

临床病例中已描述过,持续性折返性室性心动过速期间QRS波形态会出现自发改变,这种改变可逐渐或突然发生,导致心动过速呈多形性。本研究的目的是确定犬梗死模型中此类改变的机制。

方法与结果

在左前降支冠状动脉闭塞4天后的犬心脏持续性室性心动过速期间,对心外膜边界区的折返环路进行标测。在10次心动过速中,QRS波形态要么突然改变,要么逐渐改变,后者持续多达25个心动周期。当出现后者时,心电图类似尖端扭转型室速。标测结果显示,QRS波改变的主要机制是冲动离开折返环路激活心室的出口途径发生了偏移(10次心动过速中有9次)。这种偏移是由环路各段传导速度的微小变化引起的,传导速度加快或减慢,从而改变了功能性阻滞线的长度。在其中一个实验中,环路移至不同区域导致了QRS波的改变,在该实验中,折返机制也从功能性转变为解剖性。

结论

折返环路中传导的细微变化可改变QRS波形态。稳定折返环路出口途径的改变可使心电图特征类似尖端扭转型室速。

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