Waldecker B, Coromilas J, Saltman A E, Dillon S M, Wit A L
Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, N.Y. 10032.
Circulation. 1993 Apr;87(4):1286-305. doi: 10.1161/01.cir.87.4.1286.
Clinical electrophysiology studies have used, for the most part, models of anatomic reentrant circuits to explain entrainment of ventricular tachycardia. Our studies use activation maps to directly determine mechanisms of entrainment of functional circuits that cause tachycardia.
Electrograms were recorded from 192 sites on reentrant circuits in the epicardial border zone of canine myocardial infarcts during sustained ventricular tachycardia. Overdrive stimulation from different sites and at different cycle lengths was investigated. The reentrant circuits were shown to be functional, yet stimulated impulses could enter and repetitively reset the circuits (entrainment), demonstrating the presence of an excitable gap. Entrainment could occur from different stimulation sites with the stimulated impulses from each site activating the circuit with a different pattern. Entrainment, however, did not occur when the stimulated wave fronts obliterated the lines of functional block in the circuit. Fusion on the ECG occurred during entrainment when the stimulated impulses activated the ventricles concurrently with a previous stimulated impulse leaving the reentrant circuit at a different site. The first postpacing QRS was captured but not fused because it was caused by the last stimulated impulse emerging from the circuit. The first postpacing cycle length on the ECG was either equal to or longer than the overdrive cycle length depending on whether there was a fusion QRS during overdrive. The first postpacing cycle length at sites in the reentrant circuit equaled the pacing cycle length. At an appropriately short overdrive cycle length, stimulated impulses blocked in the circuit to terminate reentry.
Functional reentrant circuits causing ventricular tachycardia can be reset and entrained. Activation maps directly show the mechanisms.
临床电生理研究大多使用解剖折返环路模型来解释室性心动过速的拖带现象。我们的研究使用激动标测来直接确定导致心动过速的功能性环路的拖带机制。
在持续性室性心动过速期间，从犬心肌梗死心外膜边界区折返环路的192个部位记录了心电图。研究了来自不同部位和不同周期长度的超速刺激。结果显示折返环路具有功能性，但刺激冲动可进入并反复重置该环路（拖带），表明存在可兴奋间隙。来自不同刺激部位的拖带均可发生，每个部位的刺激冲动以不同模式激活环路。然而，当刺激波阵面消除了环路中的功能性阻滞线时，拖带不会发生。当刺激冲动与先前在不同部位离开折返环路的刺激冲动同时激活心室时，心电图上会出现融合现象。起搏后第一个QRS波被捕捉但未融合，因为它是由从环路中出现的最后一个刺激冲动引起的。根据超速刺激期间是否存在融合QRS波，心电图上的第一个起搏后周期长度等于或长于超速周期长度。折返环路部位的第一个起搏后周期长度等于起搏周期长度。在适当短的超速周期长度下，刺激冲动在环路中受阻以终止折返。
导致室性心动过速的功能性折返环路可被重置和拖带。激动标测直接显示了其机制。
