Modelagem da microestrutura de tecidos cardíacos

Abstract

A few decades ago the cardiac tissue was believed to be an uniformly connected continumm. Currently, it is known that the cardiac cells are connected to each other via special protein channels called gap junctions, through which the ionic current flows between neighboring cells. The cardiac cells are arranged in distinct layers of muscle fibers surrounded by extracellular space and connective tissue. The cardiac electrophysiology modeling is an important tool in understanding cardiac phenomena, such as arrythmias and other cardiac diseases. The Monodomain model is extensively used to describe the electrical activity in the heart. In this model the cardiac tissue is considered an uniformly connected continumm obtained by the application the homogenization technique. This is a reasonably approximation for normal physiological conditions, as in this case the cardiac microstructure is not so evident. On the other hand, some pathological conditions are known to modify the connectivity of the tissue. In isquemic and infarcted tissue it is observed a reduction in the intercellular coupling representing a partial barrier to the electrical propagation. In adittion, during fibrosis it is observed an excessive growth of the conective tissue, representing a total barrier to the electrical propagation. In such cases, recent simulation studies show that the Monodomain model can not reproduce such microscopic barrier effect on the electrical propagation. In this work we present some limitations of this model for the case of low intercellular coupling and also a numerical technique based on the finite element method to reproduce microscopic barrier caused by the presence of extracellular spaces and connective tissue in the cardiac tissue