Cardiac arrhythmias are associated with problems in the propagation of the cellular transmembrane potential, leading to the formation and, eventually, destabilization of rotors (spiral or scroll waves). To study this transition, mechanical contraction is usually neglected, being considered to be a passive consequence of electrical activity. In cardiac muscle, electrophysiological changes initiate mechanical contraction in the heart, there is also a feedback system whereby mechanical deformations (e.g. stretch) can modulate electric activity. This is called mechanoelectric feedback (MEF), and is mediated by stretch-activated channels (SAC) in the cellular membrane. The particulars of the interplay between excitation and contraction are very complex, involving the dynamics of transmembrane potential, ionic currents, intracellular calcium concentration, SAC currents, and fibers strain and stress. To gain insight into the possible pro-arrhythmic effects of mechanoelectric feedback, our approach is to consider and analyze in detail, simple models which contain the basic dynamical ingredients of MEF.

We plan to gain further insight into the effect of mechano-electrical coupling incorporating a simplified model for calcium dynamics, first to the two-variable Nash-Panfilov model, and then to a semiphysiological model of the action potential (Fenton-Karma model). This will allow us to study more complex dynamics, such as the effect of electromechanical coupling during an alternans rhythm, that is known to produce spiral break-up.