Activation delay in healed myocardial infarction: a comparison between model and experiment.
Conduction delay in healed myocardial infarction, facilitating reentry, is frequently based on an increased path length the activation has to travel in a matrix of merging and diverging bundles that survive in the infarcted area. Additional delay occurs at sites where bundles bifurcate. The purpose of this study was to investigate conduction delay at sites where bundles bifurcate. A computer model was developed to simulate spread of activation in a two-dimensional sheet of excitable elements. A structure consisting of two isolated bundles merging into a single one was modeled. Extracellular electrograms calculated in the model were comparable to electrograms obtained in a superfused infarcted papillary muscle model. A zone of crowded isochrones or local conduction delay was found at the site where an isolated bundle bifurcated. The position of the isochrones in this area depended on the way activation times were determined. Lines of activation delay were mainly perpendicular to the fiber direction. In conclusion, the results have enabled us to better understand extracellular electrograms at pivoting points and show that activation sequences at a microscopic level can best be constructed on the basis of Laplacian signals.
D003198:Computer Simulation; D004594:Electrophysiology; D005110:Extracellular Space / Q000502:physiology; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D007424:Intracellular Fluid / Q000502:physiology; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000503:physiopathology*; D009431:Neural Conduction