| A three-dimensional cellular automaton to study electrical propagation in the heart was constructed using an anatomically accurate canine ventricular geometry. Anisotropy of propagation was simulated using the actual fiber directions digitized from a canine heart.; In order to show that an anatomically accurate model could simulate activation and propagation phenomena in normal canine hearts, the heart geometry was aligned to an experimentally recorded data set, and epicardial activation isochrones for the first 50 ms were statistically compared from 45 different epicardial sites. The simulated isochrones closely resembled the experimental data both visually and statistically. Physiological values for the principal propagation velocities along the fiber, across the fiber, and across the plane formed by the fibers were also obtained.; Vulnerability to fibrillation in the model was assessed with respect to the refractory period, cycle length and anisotropic propagation. It was shown that short refractory periods, inhomogeneous distributions in the refractory periods and cycle lengths increased the vulnerability to fibrillation. Anisotropy increased the vulnerability to fibrillation in the presence of an increased inhomogeneity in the cycle lengths.; A possible mechanism for Torsades de Pointes, a ventricular tachyarrhythmia, was examined by assigning refractory periods with a smooth epicardial to endocardial gradient. A specific pacing protocol initiated self-terminating, migrating reentry in the model. The electrograms generated from the simulated data displayed the characteristic changes in the QRS morphology seen during Torsades de Pointes. The heart rates calculated from the electrograms were similar to clinically reported values. |
