It has been poorly understood whether inflammation may contribute to atrial structural remodeling and increase the propensity for atrial fibrillation (AF) to persist. We investigated the relationship between C-reactive protein (CRP) elevation and the development of atrial remodeling in AF. The study population comprised 50 consecutive paroxysmal AF (PAF) patients and 50 control patients without AF. All patients underwent echocardiography, and high-sensitivity CRP was routinely measured. C-Reactive protein was significantly higher in the patients with PAF than control patients (0.231+/-0.176 mg/dl vs 0.055+/-0.041 mg/dl, P<0.001). Other predictors of elevated CRP included left ventricular mass (P<0.05), left ventricular end-systolic diameter (P<0.05), and left atrial (LA) diameter (P<0.001). In a multivariate analysis, only CRP and LA diameter were independent predictors of PAF. Elevated CRP levels correlated with LA diameter (r=0.489, P<0.001). Left atrial diameter was increased in PAF patients compared with control patients (P<0.001). We found that a longer duration of AF is associated with higher CRP levels and a larger LA diameter (duration <30 days: CRP 0.166+/-0.139 mg/dl, LA diameter 38.4+/-8.0 mm; duration >30 days: CRP 0.345+/-0.181 mg/dl, LA diameter 45.6+/-6.6 mm; P<0.001). In conclusion, longer AF duration is associated with CRP elevation and atrial structural remodeling, as approximated by larger LA diameter. However, CRP elevation, while correlating with LA diameter, was not an independent predictor of atrial structural remodeling. Thus, it remains unclear whether CRP and the inflammatory state are contributory to LA remodeling or whether LA remodeling or AF induces elevation in CRP and inflammation.