The goal of this study is to investigate the mechanisms responsible for the increase in the upper limit of vulnerability (ULV; highest shock strength that induces arrhythmia) following the increase in pacing rate. To accomplish this goal, the study employs a three-dimensional bidomain finite element model of a slice through the canine ventricles. The preparation was paced eight times at a basic cycle length (BCL) of either 80 or 150 ms followed by delivery of shocks of various strengths and timings. Our results demonstrate that the shock strength, which induced an arrhythmia 50% of the time, increased 20% for the faster pacing compared to the slower pacing. Analysis of the mechanisms underlying the increased vulnerability revealed that delayed post-shock activations originating in the tissue depths appear as breakthrough activations on the surfaces of the preparation following an isoelectric window (IW). However, the IW duration was consistently shorter in the faster-paced preparation. Consequently, breakthrough activations appeared on the surfaces of this preparation earlier, when the tissue was less recovered, resulting in higher probability of unidirectional block and reentry. This explains why shocks of the same strength were more likely to result in arrhythmia induction when delivered to a preparation that was rapidly paced.
One contribution of 15 to a Theme Issue ‘Biomathematical modelling II’.
- © 2006 The Royal Society