Background: Brain natriuretic peptide(BNP) levels have been reported to fall following cardioversion of atrial fibrillation (AF). The mechanism for the fall in BNP has not been elucidated and the potential confounding effects of sedation have not been investigated. Sedation may alter BNP levels via its effects on loading conditions. Accordingly,we studied whether BNP levels change shortly after cardioversion and attempted to control for possible effects of sedation. Methods: BNP levels were obtained before and after cardioversion in patients with AF and in a control group of patients undergoing intravenous conscious sedation for transesophageal echocardiography. Results: BNP levels dropped (260±255 vs. 190±212 pg/ml, p< 0.05) 40 min after cardioversion, decreasing in 33 of 41 subjects who achieved sinus rhythm. By contrast, mean BNP did not fall in subjects in whom cardioversion was not successful. The change in BNP level was not related to the degree of change in heart rate. No control subject experienced a change in cardiac rhythm; BNP levels increased (195±407 vs. 238±458 pg/ml, p< 0.05) in 18/22 subjects after sedation. Baseline BNP levels were elevated in subjectswithAF, andBNP levelswere elevated in parallelwith heart failure symptoms. Conclusions: The rapid fall in BNP after cardioversion (1) may reflect prompt hemodynamic improvement associatedwith rhythmchange and (2) does not appear to be due to the effects of sedation. Background: Brain natriuretic peptide (BNP) levels have been reported to fall following cardioversion of atrial fibrillation (AF). The mechanism for the fall in BNP has not been elucidated and the potential confounding effects of sedation have not been investigated. Sedation may alter BNP Levels via its effects on sedation. Methods: BNP levels were obtained before and after cardioversion in patients with AF and in a control group of patients undergoing intravenous conscious sedation for transesophageal echocardiography. Results: BNP levels dropped (260 ± 255 vs. 190 ± 212 pg / ml, p <0.05) for 40 min after cardioversion, decreasing in 33 of 41 subjects who achieved sinus rhythm. By contrast, mean BNP did not fall in subjects in whom cardioversion was not successful. The change in BNP level was not related to the degree of change in heart rate. No cont BNP levels increased (195 ± 407 vs. 238 ± 458 pg / ml, p <0.05) in 18/22 subjects after sedation. BNP levels were elevated in subjects with AF, and BNP levels were elevated in parallelwith Conclusions: The rapid fall in BNP after cardioversion (1) may reflect prompt hemodynamic improvement associated with rhythm change and (2) does not appear to be due to the effects of sedation.