The influence of stretch-activated channels on defibrillation

Passive filling of the ventricles during fibrillation could engage stretch-activated ionic channels, which, in their turn, may alter the dynamics of fibrillation or defibrillation. We quantify the electrophysiological changes in myocardial tissue associated with the recruitment of stretch-activated channels and assess their effects on termination of a reentrant wavefront in a computational model. Our analysis reveals that stretch-activated channels elevate the resting potential, shorten the refractory period, increase propagation velocity, and alter the efficacy of shocks in terminating an arrhythmia. Most importantly, the involvement of stretch-activated channels causes the defibrillation dose-response curve to flatten; weak shocks are slightly more likely to succeed while strong shocks are more likely to fail.