Propagation of depolarization and repolarization processes in the myocardium--an anisotropic model.
A three-dimensional finite-elements model of the left and right ventricles has been developed to study the process of myocardial electrical activation. The experimentally measured velocity is known to depend on membrane processes, the cellular shape, fiber orientation, and the interaction with neighboring cells. The simulated process is, therefore, governed by the geometry and by the directional conduction velocity at each point in the myocardial volume. The geometry of the ventricles is described by ellipsoidal shape, and divided to layers and sections, each filled with "cells" of preassigned properties. It allows for taking into account the local orientation of the myocardial fibers and their distributed velocities and refractory periods. The values are Gaussly distributed around the mean, and the mean and variance differ at each section. A conduction network of Purkinje "cells" is included on the endocardial surface. The anisotropic properties are demonstrated during simulation of an abnormal cardiac cycle, when propagating is initiated at an ectopic ventricular site. Ischemia is simulated by low conduction velocities in the ischemic zone and wide dispersion of values in nearby locations; automaticity is described by restimulating "cells" in the injured area; the dangerous effects of a premature beat leading to reentry are simulated by reduction of propagation velocity in "cells" that are reactivated while they repolarize. The different activation patterns are calculated throughout the myocardium and on its surface. The generated surface activation maps are not sensitive to minute changes in location of the foci of activation within the normal conduction system. The maps show sensitivity to pathological velocities, ischemic areas, and the existence of ectopic foci.(ABSTRACT TRUNCATED AT 250 WORDS)
PubMed Abstracts
PubMed Abstracts