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Purpose <p>Atrial fibrillation (AF) is both influenced by and contributes to atrial structural remodelling, including atrial enlargement and fibrosis. In this work, we aimed to understand how differences in atrial anatomy affect AF inducibility and dynamics, both without and with fibrosis, through in silico models.</p> Methods <p>Atrial wall anatomies from late gadolinium-enhanced magnetic resonance imaging (LGE-MRI) were used to generate personalised models. Detailed intra- and inter-atrial structures (pectinate muscles, Bachmann’s bundle, fossa ovalis, coronary sinus, and fibre orientations) were mapped onto patient-specific atrial anatomies through a novel strategy using universal atrial coordinates and a highly detailed reference model. Patient-specific endomysial fibrosis was incorporated based on LGE-MRI. We quantified AF and macro-reentrant atrial tachycardia (MRAT) initiation rates in models with and without fibrosis, comparing reentry dynamics using renewal theory.</p> Results <p>We generated personalised models of 10 patients, all but one with low-fibrotic content (Utah stages ≤ 2). Anatomical variability did not significantly affect AF initiation rates in both non-fibrotic (54.0 ± 13.7%, <i>p</i> = 0.43) and fibrotic models (53.5 ± 15.3%, <i>p</i> = 0.37). For AF + MRAT, initiation rates varied significantly among fibrotic models (<i>p</i> = 0.04) but not among non-fibrotic ones (<i>p</i> = 0.14). Reentry formation rates varied significantly across anatomies both with and without fibrosis (<i>p</i> &lt; 0.04). With fibrosis, reentry destruction rates also varied significantly (<i>p</i> &lt; 0.02). The number of simultaneous reentries varied significantly across patient anatomies (<i>p</i> &lt; 0.001 without fibrosis, <i>p</i> &lt; 0.05 with fibrosis), with fibrosis altering reentry counts in 2 patients (<i>p</i> &lt; 0.02).</p> Conclusion <p>Atrial anatomy influenced patient-specific variability in AF reentry dynamics, while fibrosis played a limited modifying role in this low-fibrotic cohort.</p>

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Analysis of the Effect of Anatomical Variability on Atrial Fibrillation Dynamics Through a Novel Framework for Personalised Atrial Model Generation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月9日

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  • Victor Gonçalves Marques,
  • Ali Gharaviri,
  • Simone Pezzuto,
  • Eduard Guasch,
  • Lluís Mont,
  • Pietro Bonizzi,
  • Stef Zeemering,
  • Ulrich Schotten

摘要

Purpose

Atrial fibrillation (AF) is both influenced by and contributes to atrial structural remodelling, including atrial enlargement and fibrosis. In this work, we aimed to understand how differences in atrial anatomy affect AF inducibility and dynamics, both without and with fibrosis, through in silico models.

Methods

Atrial wall anatomies from late gadolinium-enhanced magnetic resonance imaging (LGE-MRI) were used to generate personalised models. Detailed intra- and inter-atrial structures (pectinate muscles, Bachmann’s bundle, fossa ovalis, coronary sinus, and fibre orientations) were mapped onto patient-specific atrial anatomies through a novel strategy using universal atrial coordinates and a highly detailed reference model. Patient-specific endomysial fibrosis was incorporated based on LGE-MRI. We quantified AF and macro-reentrant atrial tachycardia (MRAT) initiation rates in models with and without fibrosis, comparing reentry dynamics using renewal theory.

Results

We generated personalised models of 10 patients, all but one with low-fibrotic content (Utah stages ≤ 2). Anatomical variability did not significantly affect AF initiation rates in both non-fibrotic (54.0 ± 13.7%, p = 0.43) and fibrotic models (53.5 ± 15.3%, p = 0.37). For AF + MRAT, initiation rates varied significantly among fibrotic models (p = 0.04) but not among non-fibrotic ones (p = 0.14). Reentry formation rates varied significantly across anatomies both with and without fibrosis (p < 0.04). With fibrosis, reentry destruction rates also varied significantly (p < 0.02). The number of simultaneous reentries varied significantly across patient anatomies (p < 0.001 without fibrosis, p < 0.05 with fibrosis), with fibrosis altering reentry counts in 2 patients (p < 0.02).

Conclusion

Atrial anatomy influenced patient-specific variability in AF reentry dynamics, while fibrosis played a limited modifying role in this low-fibrotic cohort.