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Atrial fibrillation (AF) is an emerging epidemic of cardiovascular disease (CVD), being responsible for approximately 1% of the National Health Service budget of the United Kingdom.1 AF is linked to both increased morbidity (eg from ischaemic stroke, heart failure and dementia) and mortality.2 Consequently, the quest to elucidate the complexities of AF pathogenesis and perpetuation continues at a great pace, in the hope of developing future novel and effective therapeutic strategies.
Increasing attention has focused on the potential factors that might be involved in both the triggering and the perpetuation of AF. Inflammation has been postulated as a predisposing factor for AF, as well as its complications, including thromboembolism.2 In the first study to identify a potential link between inflammation and AF, Frustaci et al3 demonstrated evidence of focal myocarditis on left ventricular endocardial biopsies of three out of 14 patients with lone AF. The authors expanded on this initial work 6 years later by performing right atrial biopsies on 12 patients with lone AF, reporting that 67% of these showed evidence of right atrial myocarditis.4
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