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丙吡胺对束支传导阻滞患者的电生理效应。

Electrophysiological effects of disopyramide in patients with bundle branch block.

作者信息

Desai J M, Scheinman M, Peters R W, O'Young J

出版信息

Circulation. 1979 Feb;59(2):215-25. doi: 10.1161/01.cir.59.2.215.

Abstract

Electrophysiological studies were performed in 22 patients with intraventricular conduction delay before and after intravenous infusion of disopyramide (Norpace), 2 mg/kg. Mean control maximal sinus node recovery time (1039 +/- 187 msec), atrioventricular nodal conduction time (113 +/- 28 msec), and atrioventricular nodal effective refractory periods (349 +/- 67 msec) did not change significantly after administration of disopyramide (1073 +/- 284 msec, 112 +/- 31 msec, and 342 +/- 42 msec, respectively). Mean spontaneous cycle length (756 +/- 146 msec) decreased significantly 5 minutes after disopyramide (717 +/- 124 msec) (p less than 0.05), but not after 30 minutes (734 +/- 142 msec). A small but statistically significant (p less than 0.05) increase occurred after disopyramide in the mean atrial effective refractory period (259 +/- 51 to 280 +/- 53 msec), ventricular effective refractory period (253 +/- 23 to 275 +/- 33 msec), as well as the relative refractory period of the ventricular specialized conduction system (six patients) 433 +/- 78 to 479 +/- 62 msec). Although mean control infranodal conduction time (67 +/- 35 msec) increased 5 minutes after disopyramide (79 +/- 41 msec) (p less than 0.001) (18%), no spontaneous episodes of second-degree or third-degree atrioventricular block were observed. In six patients with premature ventricular depolarizations (greater than or equal to 1/min), the arrhythmia was totally abolished in four, markedly reduced in one, and remained unchanged in one. Disopyramide resulted in significant prolongation of infranodal conduction time as well as in atrial and ventricular refractoriness, but nevertheless appears to be safe in patients with bundle branch block.

摘要

对22例室内传导延迟患者在静脉输注2mg/kg丙吡胺(诺帕明)前后进行了电生理研究。丙吡胺给药后,平均对照最大窦房结恢复时间(1039±187毫秒)、房室结传导时间(113±28毫秒)和房室结有效不应期(349±67毫秒)无显著变化(分别为1073±284毫秒、112±31毫秒和342±42毫秒)。丙吡胺给药后5分钟,平均自发周期长度(756±146毫秒)显著缩短(717±124毫秒)(p<0.05),但30分钟后未缩短(734±142毫秒)。丙吡胺给药后,平均心房有效不应期(从259±51毫秒增至280±53毫秒)、心室有效不应期(从253±23毫秒增至275±33毫秒)以及心室特殊传导系统的相对不应期(6例患者,从433±78毫秒增至479±62毫秒)虽有小幅增加,但具有统计学意义(p<0.05)。尽管丙吡胺给药后5分钟平均结下传导时间(67±35毫秒)增加(79±41毫秒)(p<0.001)(增加18%),但未观察到二度或三度房室传导阻滞的自发发作。在6例室性早搏(≥1次/分钟)患者中,4例心律失常完全消失,1例明显减轻,1例无变化。丙吡胺导致结下传导时间以及心房和心室不应期显著延长,但对束支传导阻滞患者似乎仍属安全。

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