Simulating reentrant mechanisms under structural remodeling: A computational model based on complex-order operators

Atrial fibrillation (AF) is the most prevalent sustained cardiac arrhythmia and is strongly associated with electrical and structural remodeling. Fibrosis, a hallmark of structural remodeling, alters myocardial conduction through architectural disruption and electrotonic interactions between cardiomyocytes and fibroblasts. However, the combined effects of fibrotic texture, density, and cellular coupling on reentrant dynamics remain incompletely understood. In this work, a computational model integrating electrical and structural remodeling is used to investigate how different fibrotic architectures and degrees of heterogeneity influence reentrant mechanisms during AF. A two-dimensional atrial tissue model was implemented using a complex-order monodomain formulation to represent structural heterogeneities. Electrotonic coupling between cardiomyocytes and fibroblasts was incorporated using biophysically detailed ionic models. Compact, diffuse, and patchy fibrosis textures were simulated, including scenarios representing clinical Utah classification fibrosis densities. Reentrant activity was induced using an S1-S2 stimulation protocol and analyzed through phase singularity tracking and virtual electrograms. Simulations showed that reentrant waves anchor to fibrotic regions, with dynamics dependent on fibrotic texture, density, and complex derivative order. Increased heterogeneity and fibroblast coupling modulated dominant frequency, wave stability, and phase singularity trajectories. Quantitative analysis further showed that the imaginary part of the complex order increased the variability of activation dynamics while preserving the spatial organization of reentrant trajectories within each fibrosis configuration. Diffuse and patchy fibrosis produced heterogeneous reentry patterns, while compact fibrosis favored stable macroreentries under high fibroblast coupling.