Velocity changes in a model study of propagation in a ring of stretched ventricular myocytes

The mechanical state of the intact heart alters the electrical properties of the underlying tissue. The activity of stretch-activated transmembrane ion channels is believed to be the driving mechanism behind this mechano-electric feedback effect. Previous investigations have established that myocardial stretch reduces action potential amplitude and prolongs action potential duration, effects that may promote arrhythmias in the heart. The effect of stretch on propagation velocity, however, has not been systematically investigated. In this numerical study, action potentials propagating on a one-dimensional cable model of a ring of myocytes were analyzed for morphology changes in stretched and unstretched regions along the cable. Changes in the rest potential and action potential duration and amplitude were quantitatively similar to those observed experimentally. Propagation velocity in stretched regions was reduced by as much as twenty percent compared to the velocity in unstretched regions. This reduction in propagation velocity may play an important role in the onset and maintenance of arrhythmias induced by myocardial stretch