Activation delay in bifurcating strands of surviving myocardial
tissue in healed infarction - a comparison between model and
experiment.
Maglaveras, Nicos, Jacques M. T. De Bakker, Frans J. L. Van Capelle,
Costas Pappas, Michiel J. Janse.
Laboratory of Medical Informatics, The Medical School, Aristotelian
University, Thessaloniki, Macedonia, Greece, Department of Clinical
and Experimental Cardiology, University of Amsterdam, Academic
Medical Center, Amsterdam and the Interuniversity Cardiology
Institute, The Netherlands
APStracts 2:0233H, 1995.
Conduction delay in healed myocardial infarction, facilitating
reentry, is frequently based on an increase of the route 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 dveloped to simulate spread of activation in a 2-dimensional
sheet of excitable elements. A structure consisting of 2 isolated
bundles merging into a single one was modelled. 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 shows
that activation sequences at a microscopic level can best be
constructed on the basis of Laplacian signals.
Received 28 June 1994; accepted in final form 4 May 1995.
APS Manuscript Number H565-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.