183 Determinants of Plasma Brain Natriuretic Peptide Release in Aortic Stenosis

Abstract

Brain natriuretic peptide (BNP) is released by the left ventricle (LV) in response to increase LV wall stress and is associated with symptoms and outcome in aortic stenosis (AS). However, the relation between BNP, LV filling pressure and left atrial (LA) volume has been poorly examined in AS. This study was undertaken to assess the determinants of BNP level in AS. Two-dimensional, tissue Doppler imaging and Doppler transthoracic echocardiography were performed in 34 consecutive patients with severe AS (72±12 years, 62% of male, aortic valve area (AVA), 0.67±0.2 cm 2 , mean gradient, 45±13mmHg). Concomitantly, plasma BNP level was measured. Mean plasma level BNP was 325±572pg/ml. BNP was significantly higher in patients with reduced LV systolic function (LV ejection fraction ≤ 60%, n=22; 595±869 vs. 178±235pg/ml, p=0.04), increased indexed LA volume (≥ 40ml/m 2 , n=21; 454±686 vs. 125±210pg/ml, p=0.026) and increased LV filling pressure (E/Ea ratios: septal ≥ 15, n=17, 562±738 vs. 108±117pg/ml, p=0.004; lateral ≥ 11, n=14, 626±800 vs. 137±139, p=0.02). There were good correlations between BNP and LV and LA ejection fraction, (r=-0.40, p=0.0035 and r=-0.45, p=0.01), indexed LA volume (r=0.48, p=0.0049) and with septal and lateral E/Ea ratios (r=0.69, p<0.0001 and r=0.50, p=0.0054). However, there was lower correlation between BNP and AVA (r=0.33, p=0.047). After adjustment for age and LV ejection fraction, multivariate analysis showed that E/Ea septal (p=0.0005) or lateral (p=0.048) ratios and indexed LA volumes (p=0.006) remained associated with BNP. Furthermore, symptomatic patients (n=24) had significantly higher BNP level (427±654 vs.78±112pg/ml, p=0.009) and E/Ea septal (25±14 vs. 12±7, p=0.01) and lateral ratios (15±7 vs. 10±5, p=0.01) than asymptomatic patients. This study shows that BNP release is mainly determined by both LV and LA function in patients with AS. In this population, BNP level reflects the ventricular and atrial consequences of increased afterload rather than the severity of stenosis.