Atrial fibrillation (AF) is the most common sustained dysrhythmia in clinical practice. Despite the extensive studies, the pathophysiological mechanisms in AF, however, remain unclear. More recently, the data has been suggested that inflammatory process has been associated with development of AF. The evidence for the hypotheses included that: (1) Histological studies have demonstrated inflammatory infiltrates in AF patients and in animal models of AF; (2) inflammatory markers are increased in AF patients and is associated with successful cardioversion. And also, Inflammatory markers are not only associated with the presence of AF but also independently predicted increased risk for the development of future AF; (3) treatment with anti-inflammatory agents is associated with a decreased recurrence of AF. Although the studies suggest the existence of an association between inflammation and AF, many aspects remain elusive and require further investigation. Specifically, whether inflammation is an initiator or a perpetuator of AF; the effects of anti-inflammatory drugs on atrial remodeling and their exact role in the recurrence and perpetuation of AF. Inflammation may provide a potential target for pharmacological interruption of AF and may favorably affect atrial remodeling leading to important clinical benefits.