Left Atrial Appendage Dysfunction in Chronic Nonvalvular Atrial Fibrillation is Significantly Associated With an Elevated Level of Brain Natriuretic Peptide and a Prothrombotic State.

Abstract

trial fibrillation (AF) is associated with serious complications such as arterial thromboembolism, 1 and in patients with nonvalvular AF (NVAF) left atrial appendage (LAA) thrombi are believed to be the source of embolism. 2 In sinus rhythm, the LAA vigorously contracts with a peak emptying flow velocity greater than 50 cm/s, 3 but this is reduced in patients with chronic NVAF. 4,5 Although LAA dysfunction is a significant predictor of thrombus formation, the pathophysiologic mechanisms responsible have not been fully defined. Patients with AF are in a prothrombotic state compared with individuals in sinus rhythm. 6,7 Elevated plasma concentrations of D-dimer and thrombin -antithrombin III complex (TAT), which are markers of the intravascular activation of the coagulation system, have been found in patients with AF, 6,7 but the predictors of a hypercoagulable state in patients with NVAF have not been identified.We hypothesized that LAA dysfunction is associated with the development of a prothrombotic state and that left ventricular dysfunction leads to LAA dysfunction. The present study tested the hypothesis that LAA dysfunction would correlate with elevated levels of natriuretic peptides, which are biochemical markers of left ventricular dysfunction, 8 and with a prothrombotic state. Methods Study PopulationSixty-seven patients with a median age of 70 years (25th and 75th percentile, 65 and 74 years) with chronic NVAF between July 1999 and July 2000 were evaluated and those with a history of AF of more than 6 months duration were enrolled in the study. Patients with NVAF who had been treated with warfarin prior to transesophageal echocardiography (TEE) were excluded. Baseline clinical characteristics included age, sex, details of previous embolic events, the presence or absence of systemic hypertension, the use of aspirin, and the duration of AF. Because there were a substantial number of patients who did not have any symptoms at the onset of AF, the duration of AF was defined as the duration from the first confirmation of AF on electrocardiogram. EchocardiographyAll patients underwent transthoracic and transesophageal echocardiography. The institutional review board approved the research protocol and informed consent was obtained from all patients before undergoing TEE. The left atrial and ventricular dimensions were measured from the M-mode echocardiogram according to the recommendations of the

Who will benefit from anticoagulant therapy? Use of the CHADS2 score and its variants

“…39 Therefore, it is believed that in a patient with AF, BNP is primarily produced in the atria, whereas in a patient with heart failure, natriuretic peptide is mainly released by ventricles. 40,41 Elevated levels of BNP have been correlated with left atrial appendage dysfunction, 42,43 which itself is associated with increased risk for thromboembolic events in AF patients. 14 The prevalence of elevated biomarkers and their association with cardiovascular events in AF patients receiving chronic anticoagulation were studied independently in two clinical trials: Apixaban for the Prevention of Stroke in Subjects with Atrial Fibrillation (ARISTOTLE) and Randomized Evaluation of Long-Term Anticoagulation Therapy (RE-LY).…”

Response to Reduced Diurnal Variation of Heart Rate Is Associated With Increased Plasma B‐Type Natriuretic Peptide Level in Patients With Atrial Fibrillation

“…5 Furthermore, the plasma BNP concentration is an independent negative predictor for the LAA peak flow velocity and serves as a determinant of LAA function in nonvalvular AF. 6 In addition, Kim et al showed that the duration of AF is an independent predictor of plasma BNP levels in patients with chronic AF and preserved LV systolic function, due to the influence on the LAA peak flow velocity. 7 In conclusion, LV dysfunction is a determinant of LAA function and therefore increases BNP levels.…”

“…7 In conclusion, LV dysfunction is a determinant of LAA function and therefore increases BNP levels. 6 In addition to LV dysfunction, increased plasma BNP levels could be related to rapid progression of LAA dysfunction in patients with AF. 6 Transesophageal echocardiography can be used to identify relationships between LAA peak flow velocities, duration of AF, and plasma BNP levels.…”

“…7 In conclusion, LV dysfunction is a determinant of LAA function and therefore increases BNP levels. 6 In addition to LV dysfunction, increased plasma BNP levels could be related to rapid progression of LAA dysfunction in patients with AF.6 Transesophageal echocardiography can be used to identify relationships between LAA peak flow velocities, duration of AF, and plasma BNP levels. 8,9 If relationships between LAA peak flow velocities, duration of AF, and plasma BNP levels were identified, potential mechanisms in the relationship of heart rate variation and LV dysfunction to BNP levels could have been evaluated more precisely.…”

“…7 In conclusion, LV dysfunction is a determinant of LAA function and therefore increases BNP levels. 6 In addition to LV dysfunction, increased plasma BNP levels could be related to rapid progression of LAA dysfunction in patients with AF.…”