Abstract
Catheter ablation is a common treatment for atrial fibrillation (AF), but long-term patient outcomes remain suboptimal. Knowledge of the location of re-entrant drivers (RDs) sustaining AF can help optimize ablation strategies for individual patients. Increasing evidence suggest that both fibrosis and atrial wall thickness (A WT) can influence the RDs dynamics. This study aims to analyse the role of fibrotic patches and A WT in determining RD sites in human right (RA) and left (LA) atrial models. Atrial geometries and fibrosis distribution were obtainedfrom 2 healthy volunteers and 2 AF patients using MR imaging. These 4 subject-specific geometries were integrated into 3D atrial models with the Fenton-Karma model adopted to reproduce atrial electrophysiology. In the RA model without fibrosis, RDs anchored to the crista terminalis (CT) if initiated near a prominent AWT gradient between this bundle and surrounding RA. In the presence of fibrosis, RDs either pinned between the CT and fibrotic patch or anchored to the latter, depending on the distance from their initiation site to the CT. In the LA model without fibrosis, RDs drifted towards the thinner pulmonary veins. However, with fibrotic patches added, RDs either anchored around them or broke down into multiple wavelets. These findings can help identify RD locations from imaging data and guide ablation therapy.
Highlights
Atrial fibrillation (AF) is the most commonly sustained cardiac arrhythmia
We aim to investigate the role of atrial wall thickness (AWT) and fibrotic patches in determining anchoring of re-entrant drivers (RDs) using computational modelling performed on 3D atrial geometries and fibrosis obtained from subjectspecific magnetic resonance imaging (MRI) data
The RDs neither drifted towards the crista terminalis (CT), nor showed anchoring at any location (Figure 2E (i), F (i)). When these simulations were repeated in the presence of the synthetic fibrotic patch, the RD trajectories were affected in both subjects, as shown in (ii) columns of Figure 2
Summary
Atrial fibrillation (AF) is the most commonly sustained cardiac arrhythmia. It is characterized by complex spatiotemporal organization [1] and is associated with increased risk of heart failure and stroke [2]. The progression of AF results in ionic and structural remodelling of the atrial substrates, making RD locations harder to predict [5]. In such cases, identifying atrial RD locations requires a better understanding of the interplay between structural and functional mechanisms of AF in individual patients
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