Atrial fibrillation (AF) is the most common arrhythmia of the heart in industrialized countries. Its generation and the transitory behavior of paroxysmal AF are still not well understood. In this work we examine the interaction of two activation sources via an isthmus as possible cause for the initiation of fibrillation episodes. For this study, the electrophysiological model of Bueno-Orovio, Cherry and Fenton is adapted to atrial electrophysiology, both for physiological and electrophysiologically remodeled conditions due to AF. We show that the interaction of the pacemakers, combined with the geometrical constraints of the isthmus, can produce fibrillatory-type irregularities, which we quantify by the loss of spatial phase coherence in the transmembrane voltage. Transitions to irregular behavior occur when the frequencies of the pacemakers exceed certain thresholds, suggesting that AF episodes are initiated by frequency changes of the activating sources (sinus node, ectopic focus).
Conference Contributions (1)
C. Lenk, F. M. Weber, M. Bauer, M. Einax, G. Seemann, and P. Maass. Paroxysmal atrial fibrillation caused by interaction of pacemakerwaves and reduced excitability: Insights from the Bueno-Orovio model adapted to atria. In Computing in Cardiology Conference (CinC), pp. 1079-1082, 2013
As possible cause for atrial fibrillation (AF) we study the influence of a reduced excitability on the interaction of pacemaker waves in the Bueno-Orovio model with parameters adapted to atrial electrophysiology (aBO). One of the two pacemakers represents the sinus node and the other one a self-excitatory source in the left atrium. The pacemakers are spatially separated and their waves get in contact via a small bridge. In previous studies based on the FitzHugh-Nagumo (FHN) model it was shown that three different types of irregular activation patterns can occur in this problem. In the aBO model adapted to physiological conditions only one type is observed because, different from the FHN model, a reduction of excitability due to high-frequency pacing does not occur. If the excitability is reduced in the aBO model, all types of irregularities are recovered and, in addition, a further type is found. Because transitions from regular to irregular behavior depend on the pacing frequency, our findings provide a possible explanation for the phenomenon of paroxysmal AF.