| Rapid anti-tachycardia pacing that fails to terminate reentry might accelerate tachycardia by changing its pathway and direction, or by introducing additional waves. One pathway to acceleration of stable ventricular tachycardia is through double-wave reentry (DWR), a pacing-induced rhythm observed in dilated ventricles with shortened refractory periods.; One-dimensional ring models and a two-dimensional sheet model, containing Beeler-Reuter cells with resistive gap connections, were developed on parallel processors to investigate ventricular tachycardia (VT) caused by multiple-wave reentry (MWR): more than one wave propagating in the same direction along the same circuit simultaneously. MWR was initiated by the Si-S4/S1-S6 pacing protocols. Results indicated: (1) A vulnerable window (VW) for MWR can be opened by S3, after wave collision in the ring. The VW was located between the points of collision and stimulation, and was open for several ins 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 oil the ratio of action potential duration (ADP-60) to excitable gap (EG), 157/314, in a 1600-cell ring. (3) Continued pacing following the termination of antegrade reentry can induce retrograde reentry. (4) APD-60 was largely shortened in cellular uncoupling due to the presence of stretch-activated channels, which can provide the mechano-electrical feedback to the heart. (5) In the two-dimensional sheet model, the stable double-spiral wave can be attained after the transient fibrillation, and the wavelets formed by the wave-to-wave collisions can lead to transient fibrillation. Our models showed that the progressive acceleration of tachycardia by the addition of multiple reentrant waves traveling in the same circuit might represent a possible pathway to fibrillation. |
