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Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
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Published on: February 26, 2013

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Inflammation and C-reactive protein in atrial fibrillation: cause or effect?

Roberto Galea, Maria Teresa Cardillo, Annalisa Caroli

    Texas Heart Institute Journal
    |November 27, 2014
    PubMed

    Insights

    Inflammation may play a role in atrial fibrillation (AF) development and persistence. This review examines the complex relationship between inflammation, C-reactive protein, and AF.

    Area of Science:

    • Cardiology
    • Biomedical Science

    Background:

    • Atrial fibrillation (AF) presents significant health risks, with poorly understood causes hindering prevention.
    • A growing body of evidence links inflammation to AF.
    • Existing research presents conflicting theories on whether inflammation causes AF or if AF triggers inflammation.

    Purpose of the Study:

    • To critically review the scientific literature on the role of inflammation in atrial fibrillation.
    • To discuss the clinical significance of C-reactive protein (CRP) in the context of AF.

    Main Methods:

    • Literature review and critical analysis of existing studies.
    • Synthesis of evidence regarding the inflammation-AF connection.

    Main Results:

    • Studies show correlations between AF and inflammatory markers like C-reactive protein, myocarditis, and pericardiotomy.
    • The precise causal relationship between inflammation and AF remains debated.

    Conclusions:

    • Inflammation is implicated in the pathogenesis of atrial fibrillation.
    • Further research is needed to clarify the exact role of inflammation and C-reactive protein in AF for improved prevention and treatment strategies.

    Keywords:
    Atrial fibrillation/diagnosis/etiology/physiopathology/prevention & controlC-reactive protein/analysis/metabolismbiological markers/blooddisease managementheart conduction system/physiopathologyinflammation/complications/diagnosis/etiologymyocardial revascularization/adverse effectspolymorphism, geneticprimary preventionrisk factors

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