Effects of Wall Stress on the Dynamics of Ventricular Fibrillation: A Computer Simulation Study of Mechanoelectric Feedback

Abstract

The prevalence of ventricular fibrillation (VF) is increased in the mechanically compromised heart. Computer simulation is a useful means of investigating the mechanisms underlying this phenomenon. Using our latest research as an example, we show how computer simulations are performed and what they reveal. We have developed a fully coupled electromechanical model of the human ventricular myocardium. The model formulated the biophysics of specific ionic currents, excitation-contraction coupling, anisotropic non-linear deformation of the myocardium, and mechanoelectric feedback through stretch-activated channels. Our model suggested that sustained stretches shortens action potential duration (APD) and flattens the electrical restitution curve, whereas stretches applied at the wavefront prolongs APD. The wavefront around the core was highly stretched, even at lower pressures, resulting in a prolongation of APD and extension of the refractory area in the wavetail. As left ventricular pressures increased, the stretched area became wider and the refractory area was further extended. The extended refractory area in the wavetail facilitated wave break-up and the meandering of tips through the interaction between wavefronts and wavetails. This simulation study indicated that mechanical loading promotes meandering and wave breaks of spiral re-entry through mechanoelectric feedback. Mechanical loading in pathological conditions may contribute to the maintenance of VF through these mechanisms.