A cellular model for the simulation of activation in the ventricular myocardium.
A digital computer model of cardiac activation was used to investigate the relationship between cellular orientation and conduction and propagation of the ventricular activation wave front. The results of the simulation for  a single cycle initiated in fully recovered tissue under normal and simplified pathological conditions (ischemia and infaraction) indicate (a) that the conduction velocity of the cellular action potential in ventricular cardiac tissue may be several (3-5) times greater than is normally considered to be the case, (b) that the ventricular activation wave front propagates transmurally from endocardium to epicardium despite fiber orientation parallel to these surfaces, without the need for assuming the existence of either lateral contacts between adjacent cells or fibers with a transmural orientation, (c) the wave front of activation propagates through ventricular cardiac tissue with an anisotropic phase velocity, (d) the presence of ischemia and infarction gives rise to tangential spread of activation, and (e) small subendocardial infarcts should not be considered to be electrically silent.
D000200:Action Potentials; D003201:Computers; D003327:Coronary Disease / Q000503:physiopathology; D004594:Electrophysiology; D006321:Heart / Q000502:physiology*; D006329:Heart Conduction System / Q000502:physiology* / Q000503:physiopathology; D006352:Heart Ventricles / Q000294:innervation*; D006801:Humans; D008954:Models, Biological; D009203:Myocardial Infarction / Q000503:physiopathology; D009431:Neural Conduction; D010496:Pericardium / Q000166:cytology