Mechanical induction of arrhythmias during ventricular repolarization: modeling cellular mechanisms and their interaction in two dimensions.

Nonpenetrating mechanical stimulation of the precordial chest is particularly likely to instantaneously induce sustained rhythm disturbances if timed to coincide with ventricular repolarization. A number of possible mechanisms have been proposed, including mechanoelectric feedback acting via stretch-activated ion channels. The cellular effects of such channel activation have been studied and mathematically modeled in great detail. In this study, we investigate their dynamic interaction with the trailing wave of action potential repolarization in a two-dimensional model of ventricular tissue. The model identifies how stretch activation of cation-nonselective ion channels causes ectopic excitation in fully repolarized tissue and functional block of conduction at the intersection of the mechanical stimulus and the repolarization wave end, which may give rise to both trigger and sustaining mechanisms of ventricular arrhythmia. Simulation of stretch activation of K(+)-selective ion channels alone is insufficient in causing instantaneous arrhythmia, although it may, via action potential shortening, contribute to its sustenance.