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房室结折返性心动过速时的2:1房室传导阻滞

2:1 atrioventricular block during atrioventricular node reentrant tachycardia.

作者信息

Man K C, Brinkman K, Bogun F, Knight B, Bahu M, Weiss R, Goyal R, Harvey M, Daoud E G, Strickberger S A, Morady F

机构信息

Department of Internal Medicine, University of Michigan, Ann Arbor 48109-0022, USA.

出版信息

J Am Coll Cardiol. 1996 Dec;28(7):1770-4. doi: 10.1016/S0735-1097(96)00415-9.

DOI:10.1016/S0735-1097(96)00415-9
PMID:8962565
Abstract

OBJECTIVES

The purpose of this study was to determine the incidence and to clarify the mechanism of 2:1 atrioventricular (AV) block during AV node reentrant tachycardia induced in the electrophysiology laboratory.

BACKGROUND

In patients with 2:1 AV block during AV node reentrant tachycardia, the absence of a His bundle potential in the blocked beats has been considered evidence of intranodal, lower common pathway block.

METHODS

In consecutive patients with AV node reentrant tachycardia, the incidence of 2:1 AV block and the response to atropine and a single ventricular extrastimulus was observed.

RESULTS

Persistent 2:1 AV block occurred in 13 of 139 patients with AV node reentrant tachycardia. A His bundle deflection was present in the blocked beats in eight patients and absent in five. Patients with 2:1 AV block had a shorter tachycardia cycle length than did patients without such block (mean +/- SD 312 +/- 32 vs. 353 +/- 55 ms, p < 0.01). Atropine did not alter the 2:1 block in any patient. In every patient, a single ventricular extrastimulus introduced during the tachycardia converted the 2:1 block to 1:1 conduction.

CONCLUSIONS

The incidence of induced 2:1 AV block during AV node reentrant tachycardia is approximately 10%. The lack of a response to atropine and the consistent conversion of 2:1 block to 1:1 conduction by a ventricular extrastimulus indicate that, regardless of the presence or absence of a His bundle potential in blocked beats, 2:1 block during AV node reentrant tachycardia is due to functional infranodal block.

摘要

目的

本研究旨在确定在电生理实验室诱发房室结折返性心动过速时2:1房室传导阻滞的发生率,并阐明其机制。

背景

在房室结折返性心动过速时发生2:1房室传导阻滞的患者中,阻滞搏动中希氏束电位的缺失被认为是结内、下共同通路阻滞的证据。

方法

连续观察房室结折返性心动过速患者中2:1房室传导阻滞的发生率以及对阿托品和单个心室期外刺激的反应。

结果

139例房室结折返性心动过速患者中有13例出现持续性2:1房室传导阻滞。8例患者的阻滞搏动中有希氏束波,5例没有。发生2:1房室传导阻滞的患者其心动过速周期长度短于未发生此类阻滞的患者(平均±标准差 312±32 与 353±55 毫秒,p<0.01)。阿托品对任何患者的2:1阻滞均无影响。在每位患者中,心动过速期间引入的单个心室期外刺激将2:1阻滞转变为1:1传导。

结论

房室结折返性心动过速时诱发的2:1房室传导阻滞发生率约为10%。对阿托品无反应以及心室期外刺激能使2:1阻滞持续转变为1:1传导表明,无论阻滞搏动中有无希氏束电位,房室结折返性心动过速时的2:1阻滞是由于功能性结下阻滞。

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