Relationship between B‐type natriuretic peptide and invasive haemodynamics in patients with severe aortic valve stenosis

• Main Authors: Micha T. Maeder, Lukas Weber, Peter Ammann, Marc Buser, Niklas F. Ehl, Marc Gerhard, Roman Brenner, Philipp K. Haager, Francesco Maisano, Hans Rickli
• Format: Article
• Language: English
• Published: Wiley 2020-04-01
• Series: ESC Heart Failure
• Subjects: Natriuretic peptide; Haemodynamics; Pulmonary hypertension; Aortic stenosis; Prognosis; Valve replacement
• Online Access: https://doi.org/10.1002/ehf2.12614

Abstract Aims In patients with aortic stenosis (AS), B‐type natriuretic peptide (BNP) is a prognostic marker. However, there is little information on the association between BNP and invasive haemodynamics in AS. The aim of the present study was to assess the hitherto not well‐defined relationship between BNP and invasive haemodynamics in patients with severe AS undergoing aortic valve replacement (AVR) with a view to understand the link between high BNP and poor prognosis in these patients. In particular, we were interested in the association between BNP and combined pre‐capillary and post‐capillary pulmonary hypertension (CpcPH). Methods and results BNP was measured in 252 patients (age 74 ± 10 years, 58% male patients) with severe AS [indexed aortic valve area 0.4 ± 0.1 cm2/m2 and left ventricular ejection fraction (LVEF) 57 ± 12%] the day before cardiac catheterization. Patients were followed for a median (interquartile range) period of 3.1 (2.3–4.3) years after surgical (n = 157) or transcatheter (n = 95) AVR. The prevalence of CpcPH (mean pulmonary artery pressure ≥ 25 mmHg, mean pulmonary artery wedge pressure > 15 mmHg, and pulmonary vascular resistance > 3 Wood units) was 13%. The median BNP plasma concentration was 188 (78–452) ng/L. The indexed aortic valve area was similar across BNP quartiles (P = 0.21). Independent predictors of higher BNP (ln transformed) included lower haemoglobin (beta = −0.18; P < 0.001), lower LVEF (beta = −0.20; P < 0.001), more severe mitral regurgitation (beta = 0.20; P < 0.001), higher mean pulmonary artery wedge pressure (beta = −0.37; P < 0.001), and higher pulmonary vascular resistance (beta = 0.21; P < 0.001). In a multivariate model with CpcPH rather than its haemodynamic components, CpcPH was independently associated with higher BNP (0.21; P < 0.001). Higher ln BNP was associated with higher mortality [hazard ratio 1.90 (95% confidence interval 1.33–2.71); P < 0.001] in the univariate analysis. Patients in the third and fourth BNP quartiles had a more than six‐fold risk of death compared with patients in the first and second quartiles [hazard ratio 6.29 (95% confidence interval 1.86–21.27); P = 0.003]. In the multivariate analysis, lower LVEF [hazard ratio 0.96 (95% confidence interval 0.94–0.99) per 1% increase; P = 0.01] and CpcPH [hazard ratio 4.58 (95% confidence interval 1.89–11.09); P = 0.001] but not BNP were independently associated with mortality. The areas under the receiver operator characteristics curve for BNP for the prediction of CpcPH and mortality were 0.88 and 0.74, respectively. Conclusions In patients with severe AS, higher BNP is a marker of the presence of CpcPH and its contributors. The association between BNP and such an adverse haemodynamic profile at least in part explains the ability of BNP to predict long‐term post‐AVR mortality.