We introduce the concept of a contracting excitable medium that is capable of conducting non-linear waves of excitation that in turn initiate contraction. Furthermore, these kinematic deformations have a feedback effect on the excitation properties of the medium. Electrical characteristics resemble basic models of cardiac excitation that have been used to successfully study mechanisms of reentrant cardiac arrhythmias in electrophysiology. We present a computational framework that employs electromechanical and mechanoelectric feedback to couple a three-variable FitzHugh-Nagumo-type excitation-tension model to the non-linear stress equilibrium equations, which govern large deformation hyperelasticity. Numerically, the coupled electromechanical model combines a finite difference method approach to integrate the excitation equations, with a Galerkin finite element method to solve the equations governing tissue mechanics. We present example computations demonstrating various effects of contraction on stationary rotating spiral waves and spiral wave break. We show that tissue mechanics significantly contributes to the dynamics of electrical propagation, and that a coupled electromechanical approach should be pursued in future electrophysiological modelling studies.

Background-The mechanisms that sustain ventricular fibrillation (VF) in the human heart remain unclear. Experimental models have demonstrated either a periodic source (mother rotor) or multiple wavelets as the mechanism underlying VF. The aim of this study was to map electrical activity from the entire ventricular epicardium of human hearts to establish the relative roles of these mechanisms in sustaining early human VF. Methods and Results-In 10 patients undergoing cardiac surgery, VF was induced by burst pacing, and 20 to 40 seconds of epicardial activity was sampled (1 kHz) with a sock containing 256 unipolar contact electrodes connected to a UnEmap system. Signals were interpolated from the electrode sites to a fine regular grid (100ϫ100 points), and dominant frequencies (DFs) were calculated with a fast Fourier transform with a moving 4096-ms window (10-ms increments). Epicardial phase was calculated at each grid point with the Hilbert transform, and phase singularities and activation wavefronts were identified at 10-ms intervals. Early human VF was sustained by large coherent wavefronts punctuated by periods of disorganized wavelet behavior. The initial fitted DF intercept was 5.11Ϯ0.25 (meanϮSE) Hz (PϽ0.0001), and DF increased at a rate of 0.018Ϯ0.005 Hz/s (PϽ0.01) during VF, whereas combinations of homogeneous, heterogeneous, static, and mobile DF domains were observed for each of the patients. Epicardial reentry was present in all fibrillating hearts, typically with low numbers of phase singularities. In some cases, persistent phase singularities interacted with multiple complex wavelets; in other cases, VF was driven at times by a single reentrant wave that swept the entire epicardium for several cycles. Conclusions-Our data support both the mother rotor and multiple wavelet mechanisms of VF, which do not appear to be mutually exclusive in the human heart. (Circulation. 2006;114:536-542.)