Abstract
Atrial fibrillation (AF) is the most common cardiac arrhytmia, characterized by the chaotic motion of electrical wavefronts in the atria. In clinical practice, AF is classified under two primary categories: paroxysmal AF, short intermittent episodes separated by periods of normal electrical activity; and persistent AF, longer uninterrupted episodes of chaotic electrical activity. However, the precise reasons why AF in a given patient is paroxysmal or persistent is poorly understood. Recently, we have introduced the percolation-based Christensen-Manani-Peters (CMP) model of AF which naturally exhibits both paroxysmal and persistent AF, but precisely how these differences emerge in the model is unclear. In this paper, we dissect the CMP model to identify the cause of these different AF classifications. Starting from a mean-field model where we describe AF as a simple birth-death process, we add layers of complexity to the model and show that persistent AF arises from reentrant circuits which exhibit an asymmetry in their probability of activation relative to deactivation. As a result, different simulations generated at identical model parameters can exhibit fibrillatory episodes spanning several orders of magnitude from a few seconds to months. These findings demonstrate that diverse, complex fibrillatory dynamics can emerge from very simple dynamics in models of AF.
Highlights
Atrial fibrillation (AF) is the most common cardiac arrhythmia with a growing prevalence worldwide [1]
Our results indicate that the MF model significantly underestimates the probability of inducing AF relative to the CMP model, and that the MF model does not explain the emergence of persistent AF
Inspecting the CMP model, we identify two structural mechanisms by which reentrant circuits can form with asymmetric activation rates such that the probability of entering AF exceeds the probability of returning to sinus rhythm once AF has been initiated
Summary
Atrial fibrillation (AF) is the most common cardiac arrhythmia with a growing prevalence worldwide [1]. Adaptations of the CMP model to 3D [18] and to a realistic atrial topology based on a sheep heart [36,37] have been successful at explaining a number of key clinical results and have generated a number of new hypotheses This includes the distribution of reentrant circuits in the atria, notably in the pulmonary vein sleeves and the atrial appendages, the appearance of reentrant circuits as both reentrant and focal sources, and the increased probability of ablation failure as AF becomes more persistent. We show that the difference in the probability of inducing AF and the persistence of AF between the cCMP and CMP models can be explained by a series of complex reentrant circuits that exhibit an assymetry between the probability of activating and deactivating These circuits have a special property that they require fewer successive conduction blocks to initiate fibrillation than are needed to terminate fibrillation. We put the CMP model and our results into a wider context and discuss their potential clinical impact, the limitations of our approach, and outline proposals for future work
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