Haemodynamic mechanisms and long‐term prognostic impact of pulmonary hypertension in patients with severe aortic stenosis undergoing valve replacement. (17th October 2018)

• Record Type: Journal Article
• Authors: Weber, Lukas; Rickli, Hans; Haager, Philipp K.; Joerg, Lucas; Weilenmann, Daniel; Brenner, Roman; Taramasso, Maurizio; Baier, Philipp; Maisano, Francesco; Maeder, Micha T.
• Is Part Of: European journal of heart failure. Volume 21:Number 2(2019)
• Page Start: 172
• Page End: 181
• Publication Date: 2018-10-17
• Subjects: Aortic stenosis -- Pulmonary hypertension -- Pre‐capillary -- Post‐capillary -- Pulmonary capacitance -- Wedge pressure; Heart failure -- Periodicals; Heart Failure -- Periodicals; Insuffisance cardiaque -- Périodiques; Heart failure; Periodicals; 616.129005
• DOI: 10.1002/ejhf.1322
• Languages: English
• ISSNs: 1388-9842

Abstract

Abstract : Aims: We aimed to investigate the prevalence, detailed invasive haemodynamics, and prognostic impact of pulmonary hypertension (PH) in severe aortic stenosis (AS). Methods and results: We studied 503 patients (mean age 74 ± 10 years) with severe AS (indexed aortic valve area 0.4 ± 0.1 cm 2 /m 2, left ventricular ejection fraction 57 ± 12%) undergoing left and right heart catheterization prior to aortic valve replacement. Median follow‐up was 3.7 (interquartile range 2.6–5.4) years. Baseline PH (mean pulmonary artery pressure ≥ 25 mmHg) was found in 239 (48%) patients: 31 patients had pre‐capillary PH [mean pulmonary artery wedge pressure (mPAWP) ≤ 15 mmHg], 144 had isolated post‐capillary PH [IpcPH; mPAWP > 15 mmHg, pulmonary vascular resistance (PVR) ≤ 3 Wood units (WU)], and 64 had combined pre‐ and post‐capillary PH (CpcPH; mPAWP > 15 mmHg, PVR > 3 WU). Patients with CpcPH had higher mortality than those with IpcPH, pre‐capillary PH, and without PH. In the multivariate analysis, CpcPH remained an independent predictor of death (hazard ratio 4.39, 95% confidence interval 2.40–8.03; P < 0.001). Patients with CpcPH had higher mPAWP (26 ± 7 vs. 22 ± 5 mmHg) and lower pulmonary arterial capacitance (1.5 ± 0.6 vs. 2.9 ± 1.2 mL/mmHg) than IpcPH patients but similar left ventricular end‐diastolic pressure (LVEDP; 25 ± 7 vs. 25 ± 7 mmHg). A smaller LVEDP–mPAWP difference was related to larger left atrial size, atrial fibrillation, and more severe mitral regurgitation. Conclusions: In patients with severe AS, PH is common but underlying mechanisms differ. Patients with CpcPH have higher mPAWP, lower pulmonary arterial capacitance, and worse survival than all other groups. Left atrial dysfunction and mitral regurgitation seem to be drivers of high mPAWP in CpcPH.