Brachmann J, Kabell G, Scherlag B, Harrison L, Lazarra R
Circulation. 1983 Feb;67(2):449-56. doi: 10.1161/01.cir.67.2.449.
We analyzed the patterns of interectopic continuous electrical activity recorded within interectopic intervals of sustained ventricular tachycardias. These arrhythmias were induced in dogs that were studied 4 days after left anterior descending coronary artery occlusion. Standard ECG leads and electrograms from the His bundle and left ventricular epicardium, both infarct and normal zone, were recorded. In 19 of 24 dogs with transmural myocardial infarction, one to three ventricular paced beats induced sustained ventricular tachycardia, characterized by continuous electrical activity between the initiating and spontaneous ectopic beat and between successive ectopic beats recorded from the epicardium over the infarct zone but not from the normal epicardium. Continuous activity consisted of discrete potentials that were reproduced in each cardiac cycle, suggesting slow conduction within a reentrant circuit. The interectopic activity was divided into three distinct temporal periods, delineated by potentials occurring at the initial portion, the mid-interectopic portion and terminal portion or exit of the slow conduction segment of the presumed reentrant circuit. In some cases, sustained ventricular tachycardia was induced only if an appropriate initial potential was engaged. Spontaneous termination of the sustained ventricular tachycardia was associated with Wenckebach-like block of conduction in the initial or exit potential. Ventricular pacing caused alteration of the interectopic patterns and resulted in cessation of the arrhythmia. Procainamide produced dose-dependent slowing of the ectopic rate due to depression of conduction in the mid-interectopic portion of the continuous electric activity. Inducibility of the sustained ventricular tachycardia was inhibited by decremental conduction in this compartment of the presumed reentry circuit. The present study uses a preparation showing sustained ventricular tachycardia that is stable and regular. Functional analysis of the various portions of the continuous electrical activity during sustained tachycardias allows further insight into the mechanisms of initiation and termination of sustained ventricular tachycardias. The ability to localize the effect of antiarrhythmic drugs on specific portions of a possible reentrant circuit may provide important correlative data for the analysis and interpretation of detailed epicardial mapping studies.
我们分析了在持续性室性心动过速的异位搏动间期内记录到的异位连续电活动模式。这些心律失常是在左前降支冠状动脉闭塞4天后对犬进行研究时诱发的。记录了标准心电图导联以及希氏束和左心室心外膜（梗死区和正常区）的电图。在24只透壁性心肌梗死犬中，19只通过1至3次心室起搏搏动诱发了持续性室性心动过速，其特征是梗死区心外膜记录到的起始异位搏动与自发异位搏动之间以及连续异位搏动之间存在连续电活动，而正常心外膜未记录到。连续活动由每个心动周期中重复出现的离散电位组成，提示折返环路内存在缓慢传导。异位活动分为三个不同的时间段，由假定折返环路缓慢传导段的起始部、异位搏动间期中部和终末部或出口处出现的电位界定。在某些情况下，只有当合适的起始电位被激发时才会诱发持续性室性心动过速。持续性室性心动过速的自发终止与起始或出口电位的文氏样传导阻滞有关。心室起搏导致异位模式改变并使心律失常终止。普鲁卡因酰胺由于抑制连续电活动异位搏动间期中部的传导而产生剂量依赖性的异位心率减慢。假定折返环路该部分的递减传导抑制了持续性室性心动过速的诱发性。本研究使用了一种表现出稳定且规则的持续性室性心动过速的制备模型。对持续性心动过速期间连续电活动各部分的功能分析有助于进一步深入了解持续性室性心动过速的起始和终止机制。确定抗心律失常药物对可能折返环路特定部分的作用的能力可能为详细的心外膜标测研究的分析和解释提供重要的相关数据。
