Session S32.5

A Model for Estimating the Anisotropy of the Conduction Velocity in Cardiac Tissue Based on the Tissue Morphology

JG Stinstra*, S Poelzing, RS MacLeod, CS Henriquez

University of Utah
Salt Lake City, UT, USA

The propagation of cardiac action potentials in the myocardium is anisotropic in nature due to the fibrous structure of cardiac tissue. A well known consequence is that propagation travels faster along the fibers than across them. What is less well characterized are the effects of changes in this tissue structure, which occur in many pathologies, on propagation. In this paper we present a three-dimensional model that can predict changes in anisotropic wavefront propagation. The geometry of the model consists of sets of cardiac myocytes with realistically varying shape and organization based upon histological parameters such as average cell cross section, average cell length, and the volume fraction of extracellular space. We present the results from four separate finite element models of cardiac tissue one pair organized especially for propagation along the fiber direction pair for propagation across the fiber direction. Each pair contained models with an intracellular volume fraction of 87% and 92%, respectively. Each of the models consisted of about 0.5 million tetrahedral elements, and each modeled a volume of about 100 realistically shaped myocytes. To simulate propagation of action potentials we solved laplace's equations inside each of the volumes within the model, and used the Luo-Rudy membrane model to describe the current flow at the interfaces between extracellular and intracellular spaces. To simulate the presence of gap junctions, we imposed a resistance at each myocyte boundary. The resulting reaction-diffusion equations were solved using an implicit scheme and an iterative solver. The model predicts that when the extracellular space shrinks the conduction speed across the fibers climbed by 12%, from 0.125 m/s to 0.14 m/s, whereas the conduction speed along the fiber decreases by 10%, from 0.38m/s to 0.34m/s. The resulting change in anisotropy ratio was by 20% from 3.0 to 2.4. With the resulting values in the range of experimental values, the model will provide a tool for studying the effect of differences in cardiac morphology on anisotropy in conduction that can supplement experimental results in understanding the microscopic mechanisms of conduction. The simulations show that conduction of action potentials parallel and perpendicular to the fibrous structure change differently in respect to morphological changes, suggesting different microscopic mechanisms.

(Abstract Control Number: 146)