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束支折返:一种无心肌或瓣膜功能障碍时的室性心动过速机制。

Bundle branch reentry: a mechanism of ventricular tachycardia in the absence of myocardial or valvular dysfunction.

作者信息

Blanck Z, Jazayeri M, Dhala A, Deshpande S, Sra J, Akhtar M

机构信息

Electrophysiology Laboratory, University of Wisconsin/Milwaukee Clinical Campus, Sinai Samaritan Medical Center.

出版信息

J Am Coll Cardiol. 1993 Nov 15;22(6):1718-22. doi: 10.1016/0735-1097(93)90602-w.

Abstract

OBJECTIVES

The aim of this study was to present bundle branch reentry as the mechanism of sustained ventricular tachycardia in the absence of myocardial or valvular dysfunction.

BACKGROUND

Previous reports have documented the relation between structural heart disease and bundle branch reentrant ventricular tachycardia. Myocardial or valvular dysfunction has thus far been recognized as the only anatomic substrate for the development of this tachycardia.

METHODS

Three patients with a wide QRS complex tachycardia underwent noninvasive and invasive cardiac evaluation and electrophysiologic studies to identify the substrate and mechanism of tachycardia. Catheter ablation of the right bundle branch using radiofrequency current was performed in each patient.

RESULTS

The patients were all men (aged 54, 34 and 72 years) who presented with presyncope, palpitation and cardiac arrest, respectively. Electrocardiography during sinus rhythm revealed nonspecific intraventricular conduction delay in all three patients. Cardiac evaluation revealed no evidence of myocardial or valvular dysfunction in any patient. The baseline HV interval was prolonged in each patient (90, 100 and 75 ms, respectively). Programmed right ventricular stimulation initiated bundle branch reentrant tachycardia with typical left (three patients) and right (one patient) bundle branch block pattern. Catheter ablation of the right bundle branch using radiofrequency current abolished bundle branch reentry in all three patients. After 26-, 13- and 8-month follow-up periods, complete right bundle branch block persisted, and all three patients remained asymptomatic without antiarrhythmic drugs.

CONCLUSIONS

Sustained bundle branch reentry can be a clinical arrhythmia in patients with no identifiable myocardial or valvular dysfunction except for isolated conduction abnormalities in the His-Purkinje system. This mechanism of tachycardia should be recognized during electrophysiologic evaluation, given the seriousness of this arrhythmia and the availability of the effective treatment.

摘要

目的

本研究旨在阐述束支折返作为无心肌或瓣膜功能障碍情况下持续性室性心动过速机制的情况。

背景

既往报道记录了结构性心脏病与束支折返性室性心动过速之间的关系。迄今为止,心肌或瓣膜功能障碍一直被认为是这种心动过速发生的唯一解剖学基础。

方法

3例宽QRS波心动过速患者接受了无创和有创心脏评估及电生理检查,以确定心动过速的基础和机制。对每位患者均采用射频电流进行右束支导管消融。

结果

患者均为男性(年龄分别为54岁、34岁和72岁),分别表现为先兆晕厥、心悸和心脏骤停。窦性心律时的心电图显示,所有3例患者均有非特异性室内传导延迟。心脏评估显示,所有患者均无心肌或瓣膜功能障碍的证据。每位患者的基线HV间期均延长(分别为90、100和75毫秒)。程序性右心室刺激引发束支折返性心动过速,呈现典型的左束支阻滞图形(3例患者)和右束支阻滞图形(1例患者)。采用射频电流对右束支进行导管消融,使所有3例患者的束支折返消失。经过26个月、13个月和8个月的随访期,完全性右束支阻滞持续存在,且所有3例患者在未使用抗心律失常药物的情况下均无症状。

结论

除希氏-浦肯野系统存在孤立性传导异常外,无明确心肌或瓣膜功能障碍的患者中,持续性束支折返可能是一种临床心律失常。鉴于这种心律失常的严重性及有效治疗方法的存在,在电生理评估过程中应认识到这种心动过速机制。

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