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静脉注射盐酸普罗帕酮在持续性室性心动过速治疗中的有限作用:电生理效应及程控心室刺激结果

Limited role of intravenous propafenone hydrochloride in the treatment of sustained ventricular tachycardia: electrophysiologic effects and results of programmed ventricular stimulation.

作者信息

Doherty J U, Waxman H L, Kienzle M G, Cassidy D M, Marchlinski F E, Buxton A E, Josephson M E

出版信息

J Am Coll Cardiol. 1984 Aug;4(2):378-81. doi: 10.1016/s0735-1097(84)80229-6.

Abstract

The electrophysiologic effects and response to programmed ventricular stimulation of intravenous propafenone, an experimental antiarrhythmic agent, were studied in a group of 14 patients with both clinical and induced sustained ventricular tachycardia. Twelve of the 14 patients had not responded to conventional antiarrhythmic drug therapy. Propafenone had no significant effect on sinus cycle length (836 +/- 170 ms before and 750 +/- 124 ms after propafenone), P wave duration (108 +/- 24 ms before and 106 +/- 23 ms after propafenone) or PR interval (181 +/- 45 ms before and 194 +/- 53 ms after propafenone). QRS duration and ventricular effective refractory periods increased significantly (109 +/- 20 to 130 +/- 21 ms and 235 +/- 24 to 256 +/- 19 ms, respectively). Ventricular tachycardia remained inducible or occurred spontaneously in 13 of 14 patients after propafenone administration. Neither mode of initiation nor mode of termination of ventricular tachycardia was predictably altered. Additional forms of ventricular tachycardia were seen in six patients. Cycle length of ventricular tachycardia was 303 +/- 73 ms before and 346 +/- 143 ms after propafenone (p = NS). In conclusion, intravenous propafenone does not significantly affect sinus rate, intraatrial conduction or atrioventricular conduction. Ventricular refractoriness and intraventricular conduction are prolonged. The mode of initiation, mode of termination and ventricular tachycardia cycle length are not predictably altered, but ventricular tachycardia occasionally occurs spontaneously after propafenone. Intravenous propafenone rarely prevents induction of ventricular tachycardia in patients with sustained ventricular tachycardia refractory to conventional antiarrhythmic agents.

摘要

在一组14例既有临床持续性室性心动过速又有诱发性持续性室性心动过速的患者中,研究了一种实验性抗心律失常药物静脉注射普罗帕酮的电生理效应及其对程序性心室刺激的反应。14例患者中有12例对传统抗心律失常药物治疗无反应。普罗帕酮对窦性周期长度(普罗帕酮给药前836±170毫秒,给药后750±124毫秒)、P波时限(普罗帕酮给药前108±24毫秒,给药后106±23毫秒)或PR间期(普罗帕酮给药前181±45毫秒,给药后194±53毫秒)均无显著影响。QRS时限和心室有效不应期显著延长(分别从109±20毫秒增至130±21毫秒和从235±24毫秒增至256±19毫秒)。14例患者中有13例在给予普罗帕酮后室性心动过速仍可诱发或自发发生。室性心动过速的起始方式和终止方式均未出现可预测的改变。6例患者出现了额外形式的室性心动过速。室性心动过速的周期长度在普罗帕酮给药前为303±73毫秒,给药后为346±143毫秒(p=无显著性差异)。总之,静脉注射普罗帕酮对窦性心率、心房内传导或房室传导无显著影响。心室不应期和心室内传导延长。室性心动过速的起始方式、终止方式和周期长度未出现可预测的改变,但普罗帕酮给药后室性心动过速偶尔会自发发生。静脉注射普罗帕酮很少能预防对传统抗心律失常药物难治的持续性室性心动过速患者诱发室性心动过速。

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