Models of ventricular arrhythmia mechanisms

Abstract

The mechanisms that initiate and sustain ventricular arrhythmias in the human heart are clinically important, but hard to study experimentally. In this study, a monodomain model of electrical activation was used to examine how dynamics of electrophysiology at the cell scale influence the surface activation patterns of VF at the tissue scale. Cellular electrophysiology was described with two variants of a phenomenological model of the human ventricular epicardial action potential. The tissue geometry was an 8.0 × 8.0 × 1.2 cm 3D tissue slab with axially symmetric anisotropy. In both cases an initial re-entrant wave fragmented into multiple wavelets of activation. The model variant with steep action potential duration restitution produced much more complex activation, with a greater average number of filaments (13.79) than the variant with less steep restitution (3.08). More complex activation was associated with proportionally fewer transmural filaments, and so the average number of epicardial wavefronts and phase singularities per filament was lower. The average number of epicardial phase singularities and wavefronts for the model variant with less steep restitution were consistent with experimental observations in the human heart. This study shows that small changes in cell scale dynamics can have a large influence on the complexity of re-entrant activation in simulated 3D tissue, as well as on the features observed on the epicardial surface.