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

Area of Science:

• Computational cardiology
• Cardiac electrophysiology
• Biophysics

Background:

• Atrial fibrillation (AF) is a common arrhythmia linked to electrical and structural remodeling.
• Fibrosis disrupts myocardial conduction, but its combined effects on reentrant dynamics are not fully understood.

Purpose of the Study:

• To investigate how fibrotic architectures, density, and fibroblast coupling influence reentrant mechanisms in AF using a computational model.
• To analyze the impact of different fibrosis textures (compact, diffuse, patchy) and heterogeneity on AF dynamics.

Main Methods:

• A 2D atrial tissue model with complex-order monodomain formulation for structural heterogeneities.
• Incorporation of electrotonic coupling between cardiomyocytes and fibroblasts using detailed ionic models.
• Simulation of various fibrosis textures and densities, inducing reentrant activity via S1-S2 stimulation and analyzing with phase singularity tracking.

Main Results:

• Reentrant waves anchor to fibrotic regions, with dynamics influenced by fibrosis texture, density, and complexity.
• Increased heterogeneity and fibroblast coupling altered dominant frequency, wave stability, and reentrant trajectories.
• Diffuse and patchy fibrosis led to heterogeneous reentry, while compact fibrosis promoted stable macroreentries with high fibroblast coupling.

Conclusions:

• Fibrotic texture, density, and fibroblast coupling significantly modulate reentrant dynamics in AF.
• Computational models integrating electrical and structural remodeling are valuable for understanding AF mechanisms.
• Findings provide insights into how fibrosis heterogeneity contributes to AF complexity and may inform therapeutic strategies.