Ischemic mechanisms after myocardial infarction in a cellular model of the cardiac conduction system

Abstract The paper presents a cellular automaton model that reproduces the microstructure and bioelectric conduction of the human heart conduction system, with particular emphasis on the sinoatrial node (SAN). The model takes into account cellular differentiation (myocytes, fibroblasts, collagen) and the presence of connexins (Cx43, Cx45, Cx40) with their assigned conduction resistance. Infarction in the head SAN area was simulated as a growing gradient affecting the biophysical properties of cells and connexin degradation. The results show that progression of infarction leads to conduction disorders in the SAN, interruption of the signal to the atria, and potential activation of an escape rhythm from the atrioventricular node. In our cellular model, we identified electrophysiological phenomena not previously described in the SAN context, including the annihilation of depolarization waves within ischemic regions, a phenomenon previously reported only in the neurophysiological literature. The model reproduces physiological mechanisms and may be useful in the analysis of pathology and testing of therapeutic strategies.