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Atrial fibrillation (AF), the most common arrhythmia in the elderly, is an independent risk factor for stroke and death. There is increasing evidence that inflammation contributes to the pathogenesis of AF. Association between high-sensitivity C-reactive protein (hs-CRP) and AF has been well described, both experimentally and clinically, and studies have shown that hs-CRP and interleukin 6 (IL-6) levels are higher in patients with AF than in control patients.1–3 Incremental elevation of hs-CRP has been observed in both paroxysmal and persistent AF.1–3 Furthermore, levels of both inflammatory CRP and IL-6 have been associated with the future development and progression of AF.1–3 Of important clinical interest is the relationship between the prothrombotic state and AF. Virchow's triad, that is, left atrial blood stasis (‘flow abnormality’), endocardial damage/dysfunction (‘vessel wall abnormality’) and hypercoagulability (‘blood constituent abnormality’), may well explain the prothrombotic state in AF. Inflammation may also play an important role in the prothrombotic state in AF by promoting endothelial dysfunction and platelet activation.2–4 Blood stasis in the fibrillating left atrial appendage is a major contributor to thrombogenesis in AF, and CRP levels are considerably elevated in patients with a dilated left atrium and poorly functioning left atrial appendage.5 These reported findings have created substantial interest in the prognostic significance of inflammatory biomarkers CRP and IL-6 in patients with AF.
In their Heart study, Hijazi et al6 undertaken to address the question whether inflammatory biomarkers CRP and IL-6 can improve risk prediction in patients with AF. Their study included about 15 000 patients with AF enrolled in the Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation trial (ARISTOTLE) trial for incident strokes. The median follow-up time was 1.9 years, and the primary endpoints included …
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