Abstract:

Atrial fibrillation (AF) is the most common cardiac arrhythmia leading to a high rate of stroke. The underlying mechanisms of initiation and maintenance of AF are not fully understood. Several findings suggest a multitude of factors to leave the atria vulnerable to AF. In this work, a rule-based approach is taken to simulate the initiation of AF in a computer model for the purpose of generating a model with which the influence of anatomical structures, electrophysiological properties of the atria and arrhythmogenic activity can be evaluated. Pulmonary vein firing has been simulated leading to AF in 65.7 % of all simulations. The excitation pattern generated resemble chaotic excitation behavior, which is characteristic for AF as well as stable reentrant circuits responsible for atrial flutter. The findings compare well with literature. In future, the presented computer model of AF can be used in therapy planning such as ablation therapy or overdrive pacing.

Abstract:

Question: The mechanisms responsible for atrial fibrillation (AF) are not completely understood. Various conduction velocities and realistic anatomical structures of the atria are implemented into a computer model showing the influence of complex anatomical structures on the initiation and maintenance of AF.Method Used: In a computer model of the Visible Female heart (National Library of Medicine, Bethseda, Maryland, USA), the initiation of AF was simulated by pulmonary vein (PV) firing. The anatomical model had a resolution of 1,696,740 tissue voxel with 0.33 mm voxel side length. 32 foci around all pulmonary veins were set. The excitation propagation was simulated using an adaptive cellular automaton. Electrophysiological parameters depending on different tissue types can be set. In this work, only the conduction velocity was reduced compared to physiological data.Results: The initiation of AF through ectopic foci creates re-entrant circuits and quasi-chaotic excitation pattern in the computer model. 8 of 16 foci in the left superior, 3 of 4 foci in the left inferior, 5 of 8 foci in the right superior and 4 of 4 foci in the right inferior PV created AF after only 1.5 s. The excitation pattern shows stable re-entrant circuits as well as chaotic behavior. A breakup of stable re-entrant circuits was also observed when simulating the pathology for 17.5 s. The other foci caused self-terminating rotors.Conclusion: Computer models of the excitation propagation of the heart can be used to simulate AF initiated by triggers in the PV. A reduction in conduction velocity caused the establishment of re-entrant circuits and quasi-chaotic behavior. The complex model of the Visible Female heart showed the importance of anatomical structures in the maintenance of AF. Future work will include an improvement of the computer model by incorporating heterogeneities of atrial tissue and an implementation of individual patient models for therapy planning.