Anatomically-Induced Fibrillation in a 3D Model of the Human Atria

Mark Potse
Inria Bordeaux Sud-Ouest


INTRODUCTION The role of repolarization heterogeneity in the initiation of atrial fibrillation (AF) has been extensively investigated with computer models, but the complex anatomical structure of the atria has so far been neglected. Therefore this study aimed to test AF inducibility in a realistic 3D model of the human atria in the absence of any repolarization heterogeneity.

METHODS Simulations were performed on a recently developed atrial model representing the thin atrial wall, thicker bundles, interatrial connections, and up to three layers of fiber orientation at 0.2 mm resolution. A monodomain reaction-diffusion model based on the Courtemanche-Ramirez-Nattel human atrial myocyte model was used to simulate propagating activation. The atria were stimulated with 14 pacing pulses at decreasing intervals. 20 simulations of 5 seconds length were performed, each time with the stimuli at a different location. Another 10 simulations were run in a model with diffuse fibrosis.

RESULTS In a normal atrial model 30% of simulations resulted in AF lasting until the end of the simulation. In the fibrotic atrial models this percentage increased to 55%. AF initiation usually occurred due to waves breaking on thick bundles. In most cases AF was characterized by one or more wildly meandering spiral waves, occasionally anchoring to anatomical obstacles. In 5 cases the AF driver became purely anatomical. The circuit provided by the coronary sinus and the two atria was used in 3 of these.

CONCLUSION The structural features of the atria, with their abrupt changes in thickness and fiber orientation, suffice to cause AF when the atria are challenged with rapid stimulation. The likelihood of this anatomy-induced AF induction increases in structurally remodeled atria.