C-reactive protein but not atrial dysfunction predicts recurrences of atrial fibrillation after cardioversion in patients with preserved left ventricular function

Objectives Maintenance of sinus rhythm after cardioversion of atrial fibrillation is a major clinical challenge also in patients with preserved left ventricular function. Subclinical inflammation and atrial strain have been recognized as important contributors to atrial fibrillation onset and perpetuation. Aim of the study was to compare the predictive role of C-reactive protein (CRP) and indices of atrial dysfunction in relation to subacute arrhythmic recurrence rate in patients with persistent atrial fibrillation and normal left ventricular ejection fraction (LVEF). Methods We studied 53 patients with a mean LVEF of 58.7 ± 6%. Left atrial diameter and area, left atrial auricle emptying velocity, N-terminal pro-b-type natriuretic peptide (NT-proBNP) and CRP levels were determined few hours before electrical cardioversion. NT-proBNP and CRP levels were also measured 1 h and 3 weeks after cardioversion. Results Subacute atrial fibrillation recurrences were documented in 18 (33.9%) patients. Whereas none of the parameters reflecting atrial dysfunction predicted arrhythmic outcome, higher CRP levels (>3.0 mg/l) were significantly associated with atrial fibrillation recurrences [odds ratio (OR): 1.6; 95% confidence interval (CI): 1.4–2.5; P = 0.031]. No changes in CRP levels were evident after cardioversion independently of underlying rhythm. On the contrary, NT-proBNP levels, which were correlated with left atrial auricle emptying velocity, significantly decreased only in patients who maintained sinus rhythm (from 638 ± 329 to 295 ± 261 pg/ml; P < 0.001). Conclusion The present study demonstrates that in patients with persistent atrial fibrillation and preserved LVEF, CRP level is an independent predictor of atrial fibrillation subacute recurrence rate, whereas none of the indices of atrial dysfunction is associated with arrhythmic outcome. NT-proBNP levels reflect, instead, the hemodynamic alterations secondary to arrhythmia presence.