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房室折返性心动过速中的双波折返:同侧束支阻滞发生时心动过速周期长度的反常缩短。

Double-wave reentry in orthodromic atrioventricular reciprocating tachycardia: paradoxical shortening of the tachycardia cycle length with development of ipsilateral bundle branch block.

作者信息

Coromilas J, Kassotis J, Dizon J, Reiffel J, Costeas C, Lipka L

机构信息

Department of Medicine, The Presbyterian Hospital, New York, New York, USA.

出版信息

J Cardiovasc Electrophysiol. 1998 Aug;9(8):845-54. doi: 10.1111/j.1540-8167.1998.tb00124.x.

Abstract

INTRODUCTION

Attempts to terminate reentrant tachyarrhythmias by rapid pacing may accelerate the tachycardia. One mechanism for acceleration is double-wave reentry, where two simultaneous wavefronts travel around the same circuit.

METHODS AND RESULTS

We report pacing acceleration of AV reciprocating tachycardia (AVRT) due to double-wave reentry in a patient with Wolff-Parkinson-White syndrome. The patient had presented with atrial fibrillation and rapid conduction across a left lateral bypass tract. Intravenous procainamide was given during electrophysiologic study because of incessant atrial fibrillation and restored sinus rhythm. Orthodromic AVRT was induced and attempts to terminate the AVRT with right ventricular pacing initiated two alternate tachycardias, both with a left bundle branch block (LBBB) morphology. The first tachycardia, as expected for bundle branch block ipsilateral to the bypass tract, had a longer cycle length (CL) than the original tachycardia (366 msec compared to 297 msec). The second tachycardia had a paradoxically shorter CL, 238 msec compared to 297 msec. Electrogram analysis revealed that the circuit traversed by the accelerated LBBB tachycardia was the same as the slower LBBB tachycardia. The activation sequence revealed two independent wavefronts, traversing this common circuit. As described previously in experimental models, double-wave reentry was initiated when an antidromic-stimulated impulse blocked before colliding with the previous orthodromic impulse, thus allowing two orthodromic impulses to circulate within the circuit.

CONCLUSION

We speculate that conduction slowing by procainamide combined with the intrinsic AV nodal delay resulted in the necessary increase in the excitable gap required to develop double-wave reentry. This is the first description of sustained double-wave reentry in humans.

摘要

引言

通过快速起搏终止折返性心动过速的尝试可能会加速心动过速。加速的一种机制是双波折返,即两个同时存在的波阵面围绕同一环路传播。

方法与结果

我们报告了1例预激综合征患者因双波折返导致房室折返性心动过速(AVRT)起搏加速的情况。该患者曾出现心房颤动并经左侧旁路快速传导。在电生理研究期间,由于持续性心房颤动给予静脉注射普鲁卡因胺并恢复窦性心律。诱发了顺向性AVRT,尝试通过右心室起搏终止AVRT引发了两种交替的心动过速,二者均呈左束支阻滞(LBBB)形态。第一种心动过速,正如旁路同侧束支阻滞所预期的那样,其周期长度(CL)比原始心动过速更长(分别为366毫秒和297毫秒)。第二种心动过速的CL却反常地更短,为238毫秒,而原始心动过速为297毫秒。心电图分析显示,加速的LBBB心动过速所经过的环路与较慢的LBBB心动过速相同。激动顺序显示有两个独立的波阵面,围绕这个共同的环路传播。如先前在实验模型中所描述的,当一个逆向刺激的冲动在与先前的顺向冲动碰撞前受阻时,就会引发双波折返,从而使两个顺向冲动在环路内循环。

结论

我们推测,普鲁卡因胺导致的传导减慢与房室结固有延迟相结合,导致了形成双波折返所需的可兴奋间隙有必要增加。这是人类持续性双波折返的首次描述。

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