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异丙肾上腺素对接受氟卡尼治疗的房室折返性心动过速患者的电生理效应。

Electrophysiologic effects of isoproterenol in patients with atrioventricular reentrant tachycardia treated with flecainide.

作者信息

Helmy I, Scheinman M M, Herre J M, Sharkey H, Griffin J C

机构信息

Department of Medicine, University of California, San Francisco 94143-0214.

出版信息

J Am Coll Cardiol. 1990 Dec;16(7):1649-55. doi: 10.1016/0735-1097(90)90315-g.

Abstract

UNLABELLED

The electrophysiologic effects of isoproterenol in patients treated with flecainide for atrioventricular (AV) reentrant tachycardia were studied to evaluate the mechanism of tachycardia inducibility after isoproterenol and the value of isoproterenol challenge as a predictor of spontaneous arrhythmia recurrence. Seventeen patients underwent electrophysiologic study before and after oral flecainide administration and after the addition of isoproterenol to flecainide. No patient had inducible sustained supraventricular tachycardia after flecainide alone. Two patients had inducible sustained and six had inducible nonsustained tachycardia after isoproterenol was added to flecainide. The patients were then followed up on the same flecainide dose they received at the time of the electrophysiologic study.

FINDINGS

  1. Flecainide treatment prolonged HV and VA intervals, and the addition of isoproterenol did not affect these variables. 2) Isoproterenol shortened anterograde and retrograde block cycle length and the refractory period of the accessory pathway and the AV node. It also decreased the tachycardia cycle length, an effect that was due solely to shortening of AV node conduction time. 3) Flecainide treatment prevented tachycardia induction by affecting retrograde conduction over the accessory pathway. Isoproterenol allowed for tachycardia induction and for more sustained episodes of tachycardia by reversing the effect of flecainide on retrograde accessory pathway conduction. 4) Tachycardia recurred during follow-up in all three patients in whom tachycardia of greater than or equal to 10 s duration was induced after isoproterenol but in no patient who had no or shorter episodes of induced tachycardia (and who did not have a change in medical regimen).

CONCLUSIONS

  1. Isoproterenol reverses flecainide-induced prolongation of block cycle length and refractory periods of the accessory pathway and AV node. 2) Isoproterenol reverses flecainide-induced prevention of tachycardia induction through reversal of the effects of flecainide on the retrograde accessory pathway. 3) The addition of isoproterenol during flecainide restudy is valuable in predicting long-term drug efficacy.
摘要

未标记

研究了异丙肾上腺素对接受氟卡尼治疗房室(AV)折返性心动过速患者的电生理效应,以评估异丙肾上腺素后心动过速诱发机制以及异丙肾上腺素激发试验作为自发性心律失常复发预测指标的价值。17例患者在口服氟卡尼前后以及在氟卡尼中加入异丙肾上腺素后进行了电生理研究。单独使用氟卡尼后,无患者可诱发出持续性室上性心动过速。在氟卡尼中加入异丙肾上腺素后,2例患者可诱发出持续性心动过速,6例患者可诱发出非持续性心动过速。然后对患者进行随访,采用他们在电生理研究时所接受的相同氟卡尼剂量。

研究结果

1)氟卡尼治疗延长了HV和VA间期,加入异丙肾上腺素后这些变量未受影响。2)异丙肾上腺素缩短了前向和逆向阻滞周期长度以及旁路和房室结的不应期。它还缩短了心动过速周期长度,这一效应完全是由于房室结传导时间缩短所致。3)氟卡尼治疗通过影响旁路的逆向传导来预防心动过速的诱发。异丙肾上腺素通过逆转氟卡尼对逆向旁路传导的作用,使得心动过速得以诱发并出现更持久的心动过速发作。4)在随访期间,所有3例在异丙肾上腺素后诱发出持续时间≥10秒心动过速的患者心动过速复发,但无心动过速发作或心动过速发作较短(且治疗方案未改变)的患者无心动过速复发。

结论

1)异丙肾上腺素可逆转氟卡尼引起的旁路和房室结阻滞周期长度及不应期的延长。2)异丙肾上腺素通过逆转氟卡尼对逆向旁路的作用,逆转了氟卡尼引起的心动过速诱发的预防作用。3)在氟卡尼再研究期间加入异丙肾上腺素对预测长期药物疗效有价值。

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