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The study of pathological cardiac conditions such as arrhythmias, a majorcause of mortality in heart failure, is becoming increasingly informed bycomputational simulation, numerically modelling the governing equations. Thiscan provide insight where experimental work is constrained by technicallimitations and/or ethical issues.  As the models become more realistic, the construction of efficient andaccurate computational models becomes increasingly challenging. In particular,recent developments have started to couple the electrophysiology models withmechanical models in order to investigate the effect of tissue deformation onarrhythmogenesis, thus introducing an element of nonlinearity into themathematical representation. This paper outlines a biophysically-detailedcomputational model of coupled electromechanical cardiac activity which usesthe finite element method to approximate both electrical and mechanical systemson unstructured, deforming, meshes. An ILU preconditioner is applied to improveperformance of the solver.  This software is used to examine the role of electrophysiology, fibrosis andmechanical deformation on the stability of spiral wave dynamics in humanventricular tissue by applying it to models of both healthy and failing tissue.The latter was simulated by modifying (i) cellular electrophysiologicalproperties, to generate an increased action potential duration and alteredintracellular calcium handling, and (ii) tissue-level properties, to simulatethe gap junction remodelling, fibrosis and increased tissue stiffness seen inheart failure. The resulting numerical experiments suggest that, for the chosenmathematical models of electrophysiology and mechanical response, introducingtissue level fibrosis can have a destabilising effect on the dynamics, whilethe net effect of the electrophysiological remodelling stabilises the system.

A computational study of the effects of remodelled electrophysiology and mechanics on initiation of ventricular fibrillation in human heart failure