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维拉帕米对房室结折返性心动过速逆向传导的影响。

Effect of verapamil on retrograde conduction in atrioventricular nodal reentrant tachycardia.

作者信息

Reddy C P, McAllister R G

出版信息

Am J Cardiol. 1984 Sep 1;54(6):535-43. doi: 10.1016/0002-9149(84)90244-3.

Abstract

Using His bundle electrograms, incremental ventricular pacing and the ventricular extrastimulus (V2) technique, the effects of intravenous verapamil, 0.2 mg/kg, on retrograde atrioventricular (AV) nodal conduction during ventricular pacing, premature ventricular stimulation (H2A2 interval) and paroxysmal supraventricular tachycardia (SVT) (H-Ae interval) were evaluated in 11 patients with AV nodal reentrant tachycardia. During the control study, SVT could be induced in all 11 patients. After verapamil administration, SVT or atrial echo beats could be induced in 5 patients. Verapamil produced ventriculoatrial (VA) block at a longer cycle length than that during the control study in 10 of 11 patients (295 +/- 27 vs 352 +/- 40 ms, p less than 0.01), but prolonged H2A2 interval in only 5 of 11 patients (37 +/- 6 vs 60 +/- 31 ms, p less than 0.05). In all 5 patients with persistence of inducible SVT or atrial echo beats after verapamil treatment, the H-Ae interval remained unchanged even though in 4 of these 5 patients VA conduction time or H2A2 interval was prolonged. Correlation between the paced cycle length which induced VA block, the shortest V1H2 interval achieved during premature ventricular stimulation and the cycle length of SVT revealed that in all instances in which verapamil induced VA block at a longer cycle length than in controls but did not prolong H2A2 or H-Ae interval, the shortest V1H2 interval and the cycle length of SVT (H-H interval) were significantly longer than the ventricular paced cycle length which produced VA block.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

采用希氏束电图、递增性心室起搏和心室期外刺激(V2)技术,对11例房室结折返性心动过速患者静脉注射0.2mg/kg维拉帕米后,其在心室起搏、室性早搏刺激(H2A2间期)和阵发性室上性心动过速(SVT)(H - Ae间期)期间对逆行房室(AV)结传导的影响进行了评估。在对照研究中,11例患者均可诱发SVT。给予维拉帕米后,5例患者可诱发SVT或房性回波搏动。维拉帕米使11例患者中的10例出现室房(VA)阻滞的周期长度长于对照研究期间(295±27 vs 352±40ms,p<0.01),但仅使11例患者中的5例H2A2间期延长(37±6 vs 60±31ms,p<0.05)。在维拉帕米治疗后仍可诱发SVT或房性回波搏动的所有5例患者中,尽管这5例患者中有4例VA传导时间或H2A2间期延长,但H - Ae间期仍保持不变。诱发VA阻滞的起搏周期长度、室性早搏刺激期间达到的最短V1H2间期与SVT的周期长度之间的相关性显示,在所有维拉帕米诱发VA阻滞的周期长度长于对照但未延长H2A2或H - Ae间期的情况下,最短V1H2间期和SVT的周期长度(H - H间期)显著长于产生VA阻滞的心室起搏周期长度。(摘要截短于250字)

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