In silico analysis of the effects of fibroblasts coupling to atrial myocytes under conditions of atrial fibrillation remodeling

Under chronic atrial fibrillation (cAF), cardiac tissue experiences electrophysiological and structural remodeling, including fibrosis. Fibrosis in the atrial tissue has an important impact on myocyte action potential (AP) and its propagation. The objective of this work is to explore fibloblasts characteristics and their impact on myocytes AP. Human atrial myocyte and fibroblast electrophysiology is simulated using mathematical models proposed by Koivumaki et al., including healthy and cAF remodeled myocytes. Cellular simulations were run using three different resting membrane potentials for the fibroblasts (RMPf and different numbers of coupled fibroblasts to a single myocyte in 0D and with different fibroblast densities in 1D. Results from single cell simulations show that myocyte's AP duration (APD) depends on both RMPf and the number of coupled fibroblasts. In 1D simulation, conduction velocity (CV) depends on RMPf and density along the strand. In conclusion, fibroblasts RMPf significantly alters myocyte AP and its propagation along cardiac tissue. Myocytes affected by cAF remodeling seem to be less sensitive to changes in fibroblasts RMPf.