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<p>Idiopathic inflammatory myopathies (IIM) are systemic autoimmune disorders that frequently involve organs beyond skeletal muscle. Cardiac manifestations are common but often subclinical, with atrial fibrillation (AF) increasingly recognized as a&#xa0;clinically relevant complication. Recent data show AF prevalence rates up to 20%, markedly exceeding those of the general population. AF occurs most prominently in polymyositis and overlap myositis but is not confined to specific autoantibody profiles. Pathogenesis reflects a&#xa0;convergence of systemic inflammation, immune-mediated myocarditis, structural atrial remodeling, and inflammation-driven amplification of cardiovascular risk factors. Molecular drivers such as IL-1β, IFN‑γ, and the NLRP3 inflammasome, as well as autoantibodies targeting cardiac ion channels, further promote electrical instability. Clinically, AF in IIM is associated with increased morbidity and mortality, including up to a&#xa0;five-fold higher risk of stroke. Diagnosis is frequently complicated by oligosymptomatic courses. A&#xa0;structured approach including history, resting ECG, echocardiography, and biomarker evaluation is essential, with prolonged rhythm monitoring indicated in suspected paroxysmal AF. While AF treatment follows cardiology guidelines, effective control of the underlying myositis is crucial. Immunosuppressive regimens may attenuate inflammation-driven cardiac remodeling. Future research should focus on biomarker-based risk stratification, targeted immunomodulation, and optimized screening strategies to improve early detection and ultimately prevent arrhythmias in this high-risk population.</p>

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Vorhofflimmern bei idiopathisch immunvermittelten Myopathien

  • 期刊论文

  • 发表日期：

    2026年1月27日

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  • Tim Wilhelmi,
  • Philipp Klemm

摘要

Idiopathic inflammatory myopathies (IIM) are systemic autoimmune disorders that frequently involve organs beyond skeletal muscle. Cardiac manifestations are common but often subclinical, with atrial fibrillation (AF) increasingly recognized as a clinically relevant complication. Recent data show AF prevalence rates up to 20%, markedly exceeding those of the general population. AF occurs most prominently in polymyositis and overlap myositis but is not confined to specific autoantibody profiles. Pathogenesis reflects a convergence of systemic inflammation, immune-mediated myocarditis, structural atrial remodeling, and inflammation-driven amplification of cardiovascular risk factors. Molecular drivers such as IL-1β, IFN‑γ, and the NLRP3 inflammasome, as well as autoantibodies targeting cardiac ion channels, further promote electrical instability. Clinically, AF in IIM is associated with increased morbidity and mortality, including up to a five-fold higher risk of stroke. Diagnosis is frequently complicated by oligosymptomatic courses. A structured approach including history, resting ECG, echocardiography, and biomarker evaluation is essential, with prolonged rhythm monitoring indicated in suspected paroxysmal AF. While AF treatment follows cardiology guidelines, effective control of the underlying myositis is crucial. Immunosuppressive regimens may attenuate inflammation-driven cardiac remodeling. Future research should focus on biomarker-based risk stratification, targeted immunomodulation, and optimized screening strategies to improve early detection and ultimately prevent arrhythmias in this high-risk population.