Systemic inflammation and left atrial thrombus in patients with non-rheumatic atrial fibrillation

SummaryBackgroundThere is an apparent link between thrombogenesis and inflammation. We hypothesized that systemic inflammation [as indicated by C-reactive protein (CRP)] would be related to the presence of left atrial (LA) thrombus in patients with atrial fibrillation (AF). To test this hypothesis, we evaluated the relationship between CRP and LA thrombus in patients with non-rheumatic AF.Methods and resultsBetween October 2004 and December 2008, 190 patients with non-rheumatic AF (122 males, age 71 ± 10 years) who underwent transesophageal echocardiography (TEE) were enrolled and analyzed. All patients were examined for presence or absence of LA thrombus by TEE. CRP was measured within 1 week before the TEE examination. LA thrombus was detected in 19 patients (10%). Hypertension, hypertensive heart disease (HHD), valvular heart disease, ticlopidine, and CRP were univariate correlates of LA thrombus. By multivariate analysis, HHD (p < 0.01), ticlopidine (p = 0.01), and CRP (p = 0.03) were independently associated with LA thrombus. A cut-off CRP value for identifying LA thrombus was 0.21 mg/dl (sensitivity: 84%, specificity: 60%, positive predictive value: 19%, and negative predictive value: 97%).ConclusionA high CRP is related to LA thrombus in patients with non-rheumatic AF.