Murakawa Y, Inoue H, Toda I, Nozaki A, Kawakubo K, Sugimoto T
Second Department of Internal Medicine, University of Tokyo, Japan.
Am Heart J. 1988 May;115(5):1037-42. doi: 10.1016/0002-8703(88)90073-7.
To elucidate the mechanisms of the arrhythmogenic and antifibrillatory action of procainamide, 24 episodes of polymorphous ventricular tachycardia were analyzed. They were induced electrically in 12 canine hearts before and after the administration of 40 mg/kg of procainamide. The isochronal maps of the epicardial activation sequence were successfully constructed by 40 simultaneously recorded bipolar electrograms in 14 of 17 episodes after procainamide. The isochronal maps showed a possible macroreentrant circuit in 12 episodes, and in four of them the functional block was noticed to have disappeared before the termination of tachycardia. This study suggests that procainamide predisposes the ventricle to reentrant tachyarrhythmias and that the dimension of the reentrant circuit induced is too large to be fragmented into multiple reentries, which results in the prevention of the development of ventricular fibrillation.
为阐明普鲁卡因胺致心律失常和抗纤颤作用的机制，分析了24例多形性室性心动过速发作情况。在给予40mg/kg普鲁卡因胺前后，对12只犬心脏进行电诱导。在17次发作中的14次，通过40个同步记录的双极电图成功构建了心外膜激动序列的等时图。等时图显示12次发作中可能存在大折返环，其中4次在心动过速终止前功能性阻滞消失。本研究提示，普鲁卡因胺使心室易于发生折返性快速心律失常，且所诱导的折返环范围过大，无法分裂成多个折返，从而预防了心室颤动的发生。
