C-reactive protein and paroxysmal atrial fibrillation: evidence of the implication of an inflammatory process in paroxysmal atrial fibrillation.

BACKGROUND

Detection of inflammation is best achieved by measurements of C-reactive protein (CRP). We investigated whether inflammation might promote the development of paroxysmal atrial fibrillation (PAF), and whether high levels of CRP are associated with an increased risk of PAF.

METHODS

We assessed the levels of CRP and other risk factors in patients with PAF of recent onset (<24 h), compared with age and sex matched controls with the same risk factors who had normal sinus rhythm. Patients with thyrotoxicosis, mitral stenosis, pulmonary emboli or pericarditis were excluded. Fifty patients with PAF and 50 control subjects were finally included. All patients received amiodarone (2.7 g over 24 hours).

RESULTS

Conversion to normal sinus rhythm was achieved within 24 h in 40 patients. CRP levels were higher (P<0.001) in the PAF group (median = 0.80, min = 0.00, max = 5.90 mg/dl) compared with controls (median = 0.04, min = 0.00, max = 0.48 mg/dl). In the PAF group CRP levels were higher (P<0.001) for patients who failed to be cardioverted (median = 2.12, min = 0.80, max = 5.90 mg/dl) compared to cardiovertors. Nevertheless, CRP levels in patients who underwent successful cardioversion (median = 0.50, min = 0.00, max = 2.53 mg/dl) were higher compared with controls (P<0.001). Finally, CRP was higher in non-cardiovertors vs. control group, p<0.001. After multivariate adjustment left atrial size (OR, 4.4) and CRP levels (OR, 3.3) were significantly associated with successful cardioversion to sinus rhythm.

CONCLUSION

These results suggest that CRP has a strong association with PAF and support the hypothesis that CRP is a potent determinant of successful cardioversion of PAF in sinus rhythm.