Numerical simulations using a bidomain model suggest that the experimentally observed time-dependent changes in anodal and cathodal refractory periods result from restricting stimulus current to <8 mA.
Mehra et al. (PACE 1980; 3:526) observed that immediately after implantation of a pacing electrode in a dog heart, the anodal refractory period (RP) is shorter than the cathodal RP, but after several weeks the anodal RP becomes longer than the cathodal RP. We examine this experiment using numerical simulations based on the bidomain model of cardiac tissue and a Beeler-Reuter membrane. Our hypothesis is that accumulation of inexcitable tissue around the electrode following implantation causes the effective size of the electrode to increase and that this increase is the mechanism underlying the change in RP. We calculate that the anodal RP is shorter than the cathodal RP for both large and small electrodes. However, for large electrodes the threshold for anode "break" stimulation is greater than 8 mA. Mehra et al. defined RP experimentally as the interval at which the threshold stimulus strength becomes greater than 8 mA. If we restrict the stimulus current in our calculations to less than 8 mA, we exclude anode break stimulation from our calculation of the RP. In that case, our results are consistent with Mehra et al. and suggest that their observation resulted from their definition of RP.
Bennett et al. (Thu,) conducted a other in Cardiac tissue electrophysiology. Numerical simulations (bidomain model and Beeler-Reuter membrane) was evaluated on Anodal and cathodal refractory periods. Numerical simulations using a bidomain model suggest that the experimentally observed time-dependent changes in anodal and cathodal refractory periods result from restricting stimulus current to <8 mA.
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