Abstract:
Background: Electrical wave-front propagation in the atria is determined by local fiber orientation. Atrial fibrillation (AF) progresses with enhanced anisotropy. We illustrate AF due to myofiber structure. Methods: A 3D rabbit atrial anatomical model at 20 µm resolution with realistic fiber orientation was constructed based on contrast-enhanced micro-CT imaging. The Fenton-Karma excitation cell model was adapted to reproduce rabbit atrial action potential period (APD) of 80 ms. Diffusivities were estimated for longitudinal (Dp = 0.0065 mm2 /ms for CV = 0.5 mm/ms) and transverse directions (Dp = 0.06 mm2 /ms for CV = 0.15 mm/ms) of the fiber orientation. The estimated diffusion constants were deployed in the 3D anisotropic atrial model (Figure) where pacing was conducted with a reducing S2 interval to facilitate initiation of atrial arrhythmia. Multiple simulations were conducted with varying values of diffusion anisotropy and stimulus locations to evaluate the role of anisotropy to evaluate propensity to initiate arrhythmia. BeatBox, a cardiac simulation package, was used throughout this work. Results: Under physiological anisotropy conditions, a rapid right atrial activation was followed by the left atrial activation. Excitation waves reached the AV border where they terminated. Upon reduction of conduction heterogeneity, re-entry was initiated by the rapid pacing and the activation of both atrial chambers was almost simultaneous. Conclusions: Myofiber orientation is an effective mechanism for regulating atrial activation. Modification of its myo-architecture is proarrhythmic.