Atrial fibrillation (AF) is a common arrhythmia and is associated with significant morbidity and mortality. The pathogenesis of AF remains incompletely understood and management remains a difficult task. Over the past decade there has been accumulating evidence implicating inflammation in the pathogenesis of AF. Inflammation appears to play a significant role in the initiation and perpetuation of AF as well as the prothrombotic state associated with AF. Inflammatory biomarkers (C-reactive protein and interleukin-6) have been shown to be associated with the future development, recurrence and burden of AF, and the likelihood of successful cardioversion. Therapies directed at attenuating the inflammatory burden appear promising. Animal and clinical studies have evaluated statins, angiotensin-converting enzyme inhibitors/angiotensin-II receptor blockers, and corticosteroids for the treatment or prevention of AF. The purpose of this review is to provide current evidence on the relationship between inflammation and AF and potential therapies available to modulate the inflammatory state in AF.