Propagation in cardiac tissue adjacent to connective tissue: two-dimensional modeling studies

The conditions for activation transmission across a region of extracellular space was demonstrated in two-dimensional preparations with results consistent with those previously seen in the one-dimensional fiber studies. In addition, one sees changes in action potential morphology which occur in the tissue nearest the connective-tissue border as well as changes in conduction velocity along the border. These results hinge on an adequate representation of the connective-tissue region achieved by careful implementation of the boundary conditions in the intracellular and interstitial spaces and the expansion of the connective-tissue discretization to a "double-tier network" description. Through a series of simulations, a clear dependence on fiber orientation is illustrated in the efficacy to transmit activation. The collision of a front with an embedded connective-tissue region was also examined. The results revealed that fibers aligned normal to a planar stimulus would more greatly disrupt the advancement of a planar front. Such pronounced disruptions have been shown to be proarrhythmic in the literature. The increasing evidence of the ability of connective tissue to transmit activation has implications in understanding spread of activation through infarcted tissues and through the healthy ventricular wall in the presence of connective-tissue sheets.

[1]  M J Janse,et al.  Electrotonic Interactions across an Inexcitable Region as a Cause of Ectopic Activity in Acute Regional Myocardial Ischemia: A Study in Intact Porcine and Canine Hearts and Computer Models , 1982, Circulation research.

[2]  F Rattay,et al.  Ways to approximate current-distance relations for electrically stimulated fibers. , 1987, Journal of theoretical biology.

[3]  J. E. Mann,et al.  Propagation Down a Chain of Excitable Cells by Electric Field Interactions in the Junctional Clefts: Effect of Variation in Extracellular Resistances, Including a "Sucrose Gap" Simulation , 1983, IEEE Transactions on Biomedical Engineering.

[4]  R. Vracko,et al.  Myocyte reactions at the borders of injured and healing rat myocardium. , 1988, Laboratory investigation; a journal of technical methods and pathology.

[5]  Capelle,et al.  Slow conduction in the infarcted human heart. 'Zigzag' course of activation. , 1993, Circulation.

[6]  A. McCulloch,et al.  A collocation-Galerkin finite element model of cardiac action potential propagation , 1994, IEEE Transactions on Biomedical Engineering.

[7]  B. Roth,et al.  Electrical stimulation of cardiac tissue: a bidomain model with active membrane properties , 1994, IEEE Transactions on Biomedical Engineering.

[8]  James P. Keener,et al.  Rotating Spiral Waves Created by Geometry , 1994, Science.

[9]  C. Henriquez Simulating the electrical behavior of cardiac tissue using the bidomain model. , 1993, Critical reviews in biomedical engineering.

[10]  L. Clerc Directional differences of impulse spread in trabecular muscle from mammalian heart. , 1976, The Journal of physiology.

[11]  P. Hunter,et al.  Laminar structure of the heart: ventricular myocyte arrangement and connective tissue architecture in the dog. , 1995, The American journal of physiology.

[12]  C. Starmer,et al.  Wavelet formation in excitable cardiac tissue: the role of wavefront-obstacle interactions in initiating high-frequency fibrillatory-like arrhythmias. , 1996, Biophysical journal.

[13]  J. Crank,et al.  A practical method for numerical evaluation of solutions of partial differential equations of the heat-conduction type , 1947 .

[14]  S. Yoshizawa,et al.  Bistable Transmission Lines , 1965 .

[15]  D DiFrancesco,et al.  A model of cardiac electrical activity incorporating ionic pumps and concentration changes. , 1985, Philosophical transactions of the Royal Society of London. Series B, Biological sciences.

[16]  C. Luo,et al.  A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction. , 1991, Circulation research.

[17]  R. Plonsey,et al.  Extracellular (volume conductor) effect on adjoining cardiac muscle electrophysiology , 1988, Medical and Biological Engineering and Computing.

[18]  R. Plonsey Action potential sources and their volume conductor fields , 1977, Proceedings of the IEEE.

[19]  R. Vracko,et al.  Basal lamina of rat myocardium. Its fate after death of cardiac myocytes. , 1988, Laboratory investigation; a journal of technical methods and pathology.