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预激综合征诱发顺向性心动过速起始时功能性束支阻滞的电生理机制。刺激方法的作用。

Electrophysiologic mechanisms of functional bundle branch block at onset of induced orthodromic tachycardia in the Wolff-Parkinson-White syndrome. Role of stimulation method.

作者信息

Lehmann M H, Denker S, Mahmud R, Tchou P, Dongas J, Akhtar M

出版信息

J Clin Invest. 1985 Oct;76(4):1566-74. doi: 10.1172/JCI112138.

Abstract

The mechanisms of aberrant conduction at the onset of induced orthodromic tachycardia in the Wolff-Parkinson-White syndrome were analyzed in 20 consecutive patients in whom this tachycardia was initiated by the atrial (A2) and/or right ventricular (V2) extrastimulus techniques. Of 13 patients in whom orthodromic tachycardia was induced by the A2 method, functional right bundle branch block occurred at tachycardia onset in four (31%) and left bundle aberrancy in two (15%), one of whom also manifested right bundle aberrancy. The occurrence of bundle branch block at the onset of tachycardia was linked to aberrant conduction of the initiating A2 impulse which, in turn, was associated with attainment of relatively short His1His2 intervals within the tachycardia initiation zone. Aberrant conduction of A2 was also more common in patients without manifest preexcitation. In contrast, of 14 patients in whom orthodromic tachycardia was induced by the V2 method, left bundle aberrancy occurred at the onset of tachycardia in 11 (79%), one of whom manifested right bundle branch block as well. Left bundle aberrancy was more likely to occur when the interval from the initiating V2 (or macro-reentrant V3) impulse to the first anterograde His deflection was less than 300 ms. This suggests that left bundle aberrancy at the onset of orthodromic tachycardia induced by the V2 method results from concealed retrograde penetration of the His-Purkinje system, with the left bundle being last to recover. Our findings provide the conceptual basis for a physiologic approach to the deliberate induction of specific types of aberrant conduction at onset of orthodromic tachycardia in patients with Wolff-Parkinson-White syndrome.

摘要

对20例通过心房(A2)和/或右心室(V2)期外刺激技术诱发正向性心动过速的预激综合征患者,分析了诱发正向性心动过速起始时异常传导的机制。在13例通过A2法诱发正向性心动过速的患者中,4例(31%)在心动过速起始时出现功能性右束支传导阻滞,2例(15%)出现左束支传导异常,其中1例同时表现为右束支传导异常。心动过速起始时束支传导阻滞的发生与起始A2冲动的异常传导有关,而这又与在心动过速起始区内达到相对较短的His1His2间期有关。A2的异常传导在无明显预激的患者中也更常见。相比之下,在14例通过V2法诱发正向性心动过速的患者中,11例(79%)在心动过速起始时出现左束支传导异常,其中1例同时表现为右束支传导阻滞。当起始V2(或大折返V3)冲动至首次顺行性希氏束波的间期小于300毫秒时,更易发生左束支传导异常。这表明V2法诱发的正向性心动过速起始时的左束支传导异常是由于希氏 - 浦肯野系统的隐匿性逆行穿透,左束支最后恢复。我们的研究结果为在预激综合征患者中,以生理学方法刻意诱发正向性心动过速起始时特定类型异常传导提供了概念基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0659/424131/efcd52a58448/jcinvest00124-0286-a.jpg

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