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<b>Abstract</b>— <p>Despite significant advances in diagnosis and treatment, atrial fibrillation remains a common cardiac arrhythmia affecting up to 2% of our world’s population. Atrial fibrillation results from complex dynamic interactions between risk factors and comorbidities that trigger a variety of atrial remodeling processes. Atrial remodeling increases the persistence of atrial fibrillation while contributing to disease progression. The variability of manifestations and the wide range of mechanisms involved in the initiation, maintenance, and progression of atrial fibrillation, as well as the associated adverse outcomes, make early identification of causative factors a major challenge for modern cardiology. Computer modeling over the past 60 years has opened new avenues for understanding mechanisms, risk prediction, and personalized therapy in the treatment of atrial fibrillation. As part of our modeling of patient-specific atrial structure from gadolinium-enhanced magnetic resonance imaging data, we investigated fibrosis as a substrate for the occurrence of re-entry from a purely electrophysiological perspective. We demonstrated the effects occurring on the patient-specific atrial structure in the case of normal electrophysiology and the electrophysiology obtained in long-term atrial fibrillation. In this work, we also compared the effects of the antiarrhythmic agent Verapamil on conduction by atrial models with different electrophysiology and fibrosis distribution.</p>

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Patient-Centered Computer Model Comparing Excitation Conduction in Normal and Long-Term Persistence of Atrial Fibrillation

  • 期刊论文

  • 发表日期：

    2025年6月13日

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  • A. P. Sinitsyna,
  • A. G. Demin,
  • M. M. Slotvitsky,
  • M. A. Popov,
  • V. A. Syrovnev,
  • V. S. Kirillova,
  • V. A. Tsvelaya,
  • S. S. Bakumenko,
  • K. I. Agladze

摘要

Abstract—

Despite significant advances in diagnosis and treatment, atrial fibrillation remains a common cardiac arrhythmia affecting up to 2% of our world’s population. Atrial fibrillation results from complex dynamic interactions between risk factors and comorbidities that trigger a variety of atrial remodeling processes. Atrial remodeling increases the persistence of atrial fibrillation while contributing to disease progression. The variability of manifestations and the wide range of mechanisms involved in the initiation, maintenance, and progression of atrial fibrillation, as well as the associated adverse outcomes, make early identification of causative factors a major challenge for modern cardiology. Computer modeling over the past 60 years has opened new avenues for understanding mechanisms, risk prediction, and personalized therapy in the treatment of atrial fibrillation. As part of our modeling of patient-specific atrial structure from gadolinium-enhanced magnetic resonance imaging data, we investigated fibrosis as a substrate for the occurrence of re-entry from a purely electrophysiological perspective. We demonstrated the effects occurring on the patient-specific atrial structure in the case of normal electrophysiology and the electrophysiology obtained in long-term atrial fibrillation. In this work, we also compared the effects of the antiarrhythmic agent Verapamil on conduction by atrial models with different electrophysiology and fibrosis distribution.