A Computational Model of Brugada Syndrome in 3D Heterogeneous Cardiac Tissue

Brugada syndrome is a genetic cardiac disorder associated with ventricular arrhythmias and sudden cardiac death. There are two classical interpretations of the ECG features and pathophysiological mechanism of the BrS: the repolarization disorder theory and the depolarization disorder theory. We employed our previously published phenomenological model of human myocytes to simulate the electrical activity of cardiac tissue in a 3D transmurally heterogeneous slab. Furthermore, we modified the model to reproduce the characteristics commonly associated to BrS action potentials. We assessed the insurgence of sustained reentry as a function of electrophysiological alterations and fibrosis distribution. Additionally, for each simulation, we computed simulated epicardial unipolar electrograms. Our results suggest that both electrophysiological and structural alterations are important factors in the induction of sustained reentry associated to BrS.