To clarify whether inflammation is a cause or consequence of atrial fibrillation (AF), we measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) before and after pharmacological cardioversion in 15 patients with paroxysmal AF. Levels of hs-CRP, IL-6, and TNF-alpha after cardioversion were significantly higher than those in controls (P < 0.05). Furthermore, the levels of these indices did not differ significantly even at 24 hours and 2 weeks after cardioversion. These results suggest that inflammation is a causative agent of paroxymal AF.