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快速心室起搏诱导的心力衰竭犬房性心动过速的局灶起源

Focal origin of atrial tachycardia in dogs with rapid ventricular pacing-induced heart failure.

作者信息

Fenelon Guilherme, Shepard Richard K, Stambler Bruce S

机构信息

Department of Medicine, West Roxbury Veterans Affairs Medical Center, Harvard Medical School, West Roxbury, Massachusetts, USA.

出版信息

J Cardiovasc Electrophysiol. 2003 Oct;14(10):1093-102. doi: 10.1046/j.1540-8167.2003.03110.x.

Abstract

UNLABELLED

Mapping and Ablation of Atrial Tachycardia in Heart Failure.

INTRODUCTION

Dogs with rapid ventricular pacing-induced congestive heart failure (CHF) have inducible atrial tachycardia (AT), with a mechanism consistent with delayed afterdepolarization-mediated triggered activity. We assessed the hypothesis that AT has a focal origin.

METHODS AND RESULTS

Twenty-one CHF dogs undergoing 3 to 4 weeks of ventricular pacing at 235 beats/min were studied. Biatrial epicardial mapping of 20 sustained AT episodes (cycle length [CL], 175 +/- 53 msec) in 5 dogs revealed an area of earliest activation in the right atrial (RA) free wall (13 episodes), RA appendage (4 episodes), or between the pulmonary veins (3 episodes). Total epicardial activation time during AT (73 +/- 19 msec) was similar to that during sinus rhythm (72 +/- 13 msec) and on average was <50% of the AT CL. Higher-density mapping of the RA free wall during 30 sustained AT episodes (163 +/- 55 msec) in 9 dogs identified a site of earliest activation along the sulcus terminalis most frequently as a stable, focal activation pattern from a single site. Endocardial mapping of 49 sustained AT episodes (156 +/- 27 msec) in 10 dogs revealed multiple sites of AT origin arising along the crista terminalis and pulmonary veins. Right and left ATs were terminated with discrete radiofrequency ablation, but other ATs remained inducible. A rapid, left AT generating an ECG pattern of atrial fibrillation was ablated inside the pulmonary vein.

CONCLUSION

AT induced in this CHF model after 3 to 4 weeks of rapid ventricular pacing has an activation pattern consistent with a focal origin. Sites of earliest activation are distributed predominately along the crista terminalis and within or near the pulmonary veins.

摘要

未标注

心力衰竭时房性心动过速的标测与消融

引言

快速心室起搏诱发充血性心力衰竭(CHF)的犬可诱发房性心动过速(AT),其机制与延迟后除极介导的触发活动一致。我们评估了AT有局灶性起源的假说。

方法与结果

对21只接受235次/分钟心室起搏3至4周的CHF犬进行了研究。对5只犬的20次持续性AT发作(周长[CL],175±53毫秒)进行双房心外膜标测,发现右心房(RA)游离壁(13次发作)、RA心耳(4次发作)或肺静脉之间(3次发作)有最早激动区域。AT期间的心外膜总激动时间(73±19毫秒)与窦性心律期间(72±13毫秒)相似,平均<AT周长的50%。对9只犬的30次持续性AT发作(163±55毫秒)期间的RA游离壁进行更高密度标测,最常确定沿终沟的最早激动部位为来自单个部位的稳定局灶性激动模式。对10只犬的49次持续性AT发作(156±27毫秒)进行心内膜标测,发现沿界嵴和肺静脉有多个AT起源部位。右房和左房的AT通过离散射频消融终止,但其他AT仍可诱发。在肺静脉内消融了一个快速的、产生心房颤动心电图模式的左房AT。

结论

在该CHF模型中,快速心室起搏3至4周后诱发的AT具有与局灶性起源一致的激动模式。最早激动部位主要分布在界嵴以及肺静脉内或附近。

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