C-reactive protein and atrial fibrillation: “Evidence for the presence of inflammation in the perpetuation of the arrhythmia”

BackgroundAtrial fibrillation (AF) is associated to a high risk of systemic embolism. The mechanisms that contribute to thrombogenesis in these patients are still poorly understood. Systemic and/or local inflammation could be involved in the process of thrombogenesis and contribute to the perpetuation of the arrhythmia. The purpose of the study was to evaluate the role of inflammation and its relation to thrombogenesis and cardiac rhythm in AF.MethodsWe prospectively studied 130 patients with newly diagnosed non-valvular AF in absence of antithrombotic therapy. Determinations of C-reactive protein (CRP) and thrombin–antithrombin complex (TAT) plasma levels, along with a transesophageal echocardiogram were performed in all the patients at admission.ResultsMean age of the group was 67 ± 14 years. CRP levels were significantly elevated in AF patients versus controls (matched by age, gender and cardiovascular risk factors) (1.0 ± 1.8 versus 0.3 ± 0.4 mg/dl, respectively, p < 0.01). Baseline TAT levels were also significantly elevated in AF patients but no correlation was found between CRP and TAT. At 1-year of follow-up, mean CRP levels were still elevated in patients that remained in AF compared to those who converted to sinus rhythm (1.2 ± 1.8 compared to 0.5 ± 1.5 mg/dl, p = 0.03). CRP was the only biochemical predictor of sinus rhythm maintenance at 1-year follow-up independently of clinical (including adjustment for risk factors and antiarrhythmic drugs), biochemical and echo parameters.ConclusionsThere is evidence for the presence of inflammation in patients with non-valvular AF, which is not related to activation of the coagulation cascade. The persistence of inflammation is associated with chronic AF at 1-year follow up.