TL;DR
This paper introduces a simple computational model that unifies the understanding of atrial fibrillation mechanisms, explaining diverse activation patterns through tissue structure and predicting ablation success variability.
Contribution
The study presents a novel, minimal model linking atrial tissue architecture to AF dynamics, providing a theoretical framework for clinical observations and treatment outcomes.
Findings
Surface activation patterns depend on tissue thickness.
Re-entrant circuits differ between paroxysmal and persistent AF.
Ablation effectiveness varies with AF type and circuit location.
Abstract
The mechanism of atrial fibrillation (AF) is poorly understood, resulting in disappointing success rates of ablative treatment. Different mechanisms defined largely by different atrial activation patterns have been proposed and, arguably, this dispute has slowed the progress of AF research. Recent clinical evidence suggests a unifying mechanism based on sustained re-entrant circuits in the complex atrial architecture. Here, we present a simple computational model showing spontaneous emergence of AF that strongly supports, and gives a theoretical explanation for, the clinically observed diversity of activation. We show that the difference in surface activation patterns is a direct consequence of the thickness of the discrete network of heart muscle cells through which electrical signals percolate to reach the imaged surface. The model naturally follows the clinical spectrum of AF…
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