Termination and acceleration of ventricular tachycardia in a propagating model

Abstract

Computer ring models of ventricular tissue were developed by parallel processing to study pacing-induced double-wave reentry (DWR) and reversal of reentry (RR). The rings contained 400-1600 Beeler-Reuter cells, coupled by resistive gaps. Reentry was initiated by the S1-S2 protocols. The conditions required for DWR and RR were studied using premature pulses S3-S4/S3-S5 during reentry. The results indicated the following: (1) To initiate DWR, S4 must occur in a new vulnerable window (VW) opened by S3, after wave collision is induced in the ring. The window is located between the points of collision and stimulation, and is open for several ms following S3. (2) Acceleration of tachycardia beyond DWR can be accomplished by adding a third reentrant wave in the same circuit, with the S3-S4 pacing protocol based on the ratio of action potential duration to excitable gap, 157/314. (3) Continued pacing S4-S5 following termination of retrograde reentry by S3 can induce antegrade reentry. (4) Termination of single-wave reentry by entrainment can succeed in a wider time period from 4 ms to 50 ms due to alternating action potential duration caused by a 5% decrease in IKr conductance. The authors' models showed progressive acceleration of tachycardia by the addition of multiple reentrant waves traveling in the same circuit, which might represent a possible pathway to fibrillation. It should be noted that the number of reentrant waves and the degree of acceleration are limited only the ratio of action potential duration to excitable gap.