Abstract

A computer model of propagated excitation and recovery in anisotropic cardiac tissue was described in the first report of this series. The model consists of a large number of excitable elements whose subthreshold interactions are governed by the anisotropic bidomain theory but whose suprathreshold behavior (action potential) is largely preassigned. As described in the first report, the model's performance was tested in rectangular and cubic arrays of excitable elements. This second report deals with three-dimensional simulations in a simplified left ventricle with anisotropy; specifically, the activation process in the “normal” ventricle is described (exemplified by the activation sequences started from various endocardial, intramural, and epicardial sites). To further substantiate our model's validity, we compare simulated epicardial and body-surface potential distributions with experimental findings in isolated canine hearts and with clinical evidence provided by electrocardiographic body-surface mapping.

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