ALTERNATIONS IN ATRIAL-NATRIURETIC-PEPTIDE RELEASE AFTER DC CARDIOVERSION OF NONVALVULAR CHRONIC ATRIAL-FIBRILLATION

The response of atrial natriuretic peptide (ANP) release to haemodynam ic influences after cardioversion of atrial fibrillation has not been fully examined. We measured plasma concentrations of ANP and assessed haemodynamic changes 60-120 min after DC cardioversion in 22 patients with non-valvular chronic atrial fibrillation. Passive leg elevation t o enhance volume expansion was performed 60 min after DC cardioversion . Sinus rhythm was restored in 18 of the 22 patients (successful DC ca rdioversion group). The control group consisted of seven patients with non-valvular chronic atrial fibrillation who did not undergo DC cardi oversion (atrial fibrillation control group). In the successful DC car dioversion group, the mean pulmonary artery wedge wedge pressure decre ased significantly 15 min after cardioversion (P<0.05) and then remain ed unchanged. Plasma concentrations of ANP also decreased significantl y 15 min after cardioversion (P<0.05). Furthermore, there was an addit ional significant decrease in ANP levels for up to 60 min after cardio version (P<0.05 from 15 min). Passive leg elevation for 15 min led to an increase in the mean pulmonary artery wedge pressure (P<0.01) and r ight atrial pressure (P<0.05), but did not result in increased plasma concentrations of AHP (47.1 +/- 27.6 vs 43.9 +/- 34.4 pg . ml(-1), mea n +/- SD, P=ns). In the atrial fibrillation control group, passive leg elevation increased the mean pulmonary artery wedge pressure (P<0.01) , the mean right atrial pressure (P<0.05) and plasma concentrations of ANP (139.9 +/- 85.8 vs 168.1 +/- 108.2, P<0.05). In summary, after su ccessful DC cardioversion of non-valvular chronic atrial fibrillation, plasma concentrations of ANP decreased in conjunction with decreased mean pulmonary artery wedge pressure. The response of ANP release to v olume expansion expansion, however, appears to be dysregulated in this patient population.