The global burden of atrial fibrillation (AF) is large and growing. AF already affects roughly 6.7 million people in the U.S. and Europe, accounting for one-third of hospitalizations for cardiac arrhythmia , 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.  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.  Other potential antifibrillatory effects of statin therapy have been proposed, including antioxidant effects, improvement in endothelial function, reduction of neurohormonal activation, and beneficial effects on atrial cellular and electrophysiological remodeling.[4,5] However, the clinical efficacy of statin therapy for prevention of AF has not been well-established, and data examining the impact of statin therapy on AF in women have been especially limited.
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