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The global burden of atrial fibrillation (AF) is large and growing. AF already affects roughly 6.7 million people in the USA and Europe, accounting for one-third of admissions to hospital for cardiac arrhythmia,1 and these figures are expected to increase progressively in coming years. While the principal pathogenetic features of AF include automatic ectopic foci in the thoracic veins and multiple wavelet generation within the left atrium, recent studies suggest that inflammation is also associated with development of AF.2 This concept has led to a growing interest in the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, as potential therapeutic agents for AF due to their potential anti-inflammatory effects.3 Other potential antifibrillatory effects of statin treatment have been proposed, including antioxidant effects, improvement in endothelial function, reduction of neurohormonal activation and beneficial effects on atrial cellular and electrophysiological remodelling.4 5 However, the clinical efficacy of statin treatment for prevention of AF has not been well established, and data examining the impact of statin treatment on AF in women have been especially limited.
In this issue of Heart, Pellegrini et al6 used the cohort of the Heart and Estrogen/Progestin Replacement Study (HERS) to investigate the effect of statin treatment on prevalence and incidence of AF in 2673 postmenopausal women with stable coronary artery disease (see article on page 704). Cross-sectional analysis of the cohort at enrolment showed a 65% lower odds of having AF in women who were receiving statin treatment, even after adjustment for potential confounding variables. Longitudinal analysis over the mean follow-up of 4.1 years showed that women taking a statin at baseline were 55% less likely to develop AF than those who were not. Combining the data, …