Abstract:

BackgroundMultiple wavelets and rotors are accused of maintaining atrial fibrillation (AF). However, snake-like excitation patterns have recently been observed in AF. So far, computer models have investigated AF in a simplified anatomical model. In this work, pulmonary vein firing is simulated to investigate the initiation and maintenance of AF in a realistic anatomical model.Methods and ResultsThirty-five ectopic foci situated around all pulmonary veins were simulated by a unidirectional conduction block. The excitation propagation was simulated by an adaptive cellular automaton on a realistic 3-dimensional atrial anatomy. Atrial fibrillation was initiated in 65.7% of the simulations. Stable excitation patterns were broken up in anatomically heterogeneous regions, creating a streak-like excitation pattern similar to snakes. Multiple wavelets and rotors could be observed in anatomically smooth areas at the atria's roofs.ConclusionsThe influence of macroscopic anatomical structures on the course of AF seems to play an important role in the excitation propagation in AF. The computer simulations indicate that multiple mechanisms contribute to the maintenance of AF.

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.

Abstract:

The purpose of this study is to develop a computer model-based planning environment for therapeutically cardiac interventions, i.e. surgical or catheter ablation procedures in atrial cases and placing pacemaker electrodes in biventricular pacing. Existing mathematical models are used to simulate the electrophysiology on an anatomical pig model during a heart cycle. The results of these models were validated in multiple domestic pig animal experiments. We found that the models created enable us to simulate the electrical behaviour of the heart nearly in real time and that it reproduces the properties of the heart in atrial flutter and in ventricular pacing with different pacing locations. The results of computer-based simulations may lead to a better understanding of cardiac rhythm disorders and the development of new, less invasive operative techniques.