Abstract 5125: Elevated Serum Brain Natriuretic Peptide Level Predicts the Presence of the Left Atrial Appendage Dysfunction in Patients With Acute Ischemic Stroke

Abstract

Background: It is well known that the left atrial appendage (LAA) dysfunction plays an important role in the occurrence of the cardioembolic stroke. It has been reported that the atrium is the main source of brain natriuretic peptide (BNP) in atrial fibrillation patients without heart failure. Therefore, we hypothesized that serum BNP levels are sensitive predictor for LAA dysfunction and thrombus formation in patients with acute ischemic stroke. Methods: We performed trans-thoracic and esophageal echocardiography within 7 days after the onset (male, n=64, 69±11 years old; female, n=38, 68±15 years old) and measured serum hemostatic markers and BNP in 103 patients with ischemic stroke. No patients had history of heart failure. Results: LAA thrombus was detected in 8 patients (36%) among 22 patients with atrial fibrillation. Even in 3 patients (4%) among 80 patients with sinus rhythm, LAA thrombus was detected. There were no significant differences in left ventricular end-diastolic dimension (LVDd), and the ratio of the early diastolic trans-mitral inflow velocity (E) to mitral annular velocity (E′) between patients with and without LAA thrombus (LVDd, 49±6 vs. 47±5 mm; E/E′, 8.6±1.3 vs. 7.2±0.9). Serum BNP levels were markedly higher in patients with LAA thrombus formation than in those without it (191 (128 –278) vs. 39 (13–100) pg/ml, P<0.01). Furthermore, in patients with sinus rhythm (n=80), the BNP levels were significantly correlated with LAA peak emptying flow velocity (R=−0.34, P<0.01). The multivariate logistic regression analysis revealed that BNP >120 was an independent predictor of LAA thrombus formation (odds ratio, 13.50; 95% confidence interval, 2.482–73.40; P=0.0026). Conclusions: The BNP levels were correlated with LAA peak emptying flow velocity. The elevated BNP level could be used as a non-invasive surrogate maker to predict LAA dysfunction and thrombus formation in patients with acute ischemic stroke.