Termination of reentrant propagation by a single extracellular stimulus in an atrial ring model

Cardiac reentry, the underlying mechanism of both tachycardia and fibrillation, is often terminated clinically with extracellular stimuli. We developed a one-dimensional mathematical model to find the probability that a short, randomly-timed extracellular stimulus would terminate reentry and to study the mechanisms responsible for termination. Our ring model consisted of 100 atrial cells, with the cell membrane represented mathematically by a model developed by Nygren et al. (1998). Stable reentry was established, and then a single extracellular stimulus with a pulsewidth of either 2.5 msec or 5.0 msec was applied through a cathode positioned over cell 25 and an anode over cell 50. Total delivered charge was kept constant. The timing of the stimulus was varied in 1.0 msec steps so as to sample one complete revolution of the reentering wavefront. The probability that the 2.5 mec stimulus would terminate reentry was 2.8%, 0.2% at the cathode and 2.6% at the anode. The probability of termination increased to 4.2% with the 5.0 msec stimulus (1.5% at the cathode and 2.7% at the anode). The anode was more significant than the cathode in terminating reentry, and the anodal mechanism was less sensitive to the stimulus pulsewidth.