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Original research
Prevalence of pulmonary hypertension in aortic stenosis and its influence on outcomes
  1. Seshika Ratwatte1,2,
  2. Simon Stewart3,4,
  3. Geoff Strange3,5,
  4. David Playford3,
  5. David S Celermajer1,2
  1. 1Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia
  2. 2School of Medicine and Health, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia
  3. 3Institute for Health Research, The University of Notre Dame Australia, Fremantle, Western Australia, Australia
  4. 4School of Medicine, Dentistry and Nursing, University of Glasgow, Glasgow, UK
  5. 5Heart Research Institute Ltd, Newtown, Sydney, Australia
  1. Correspondence to Professor David S Celermajer, Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, NSW 2050, Australia; David.Celermajer{at}health.nsw.gov.au

Abstract

Objective The significance of pulmonary hypertension (PHT) complicating aortic stenosis (AS) is poorly characterised. In a large cohort of adults with at least moderate AS, we aimed to describe the prevalence and prognostic importance of PHT in such patients.

Methods In this retrospective study, we analysed the National Echocardiography Database of Australia (data from 2000 to 2019). Adults with an estimated right ventricular systolic pressure (eRVSP), left ventricular ejection fraction (LVEF) >50% and with moderate or greater AS were included (n=14 980). These subjects were then categorised according to their eRVSP. The relationship between PHT severity and mortality outcomes were evaluated (median follow-up of 2.6 years, IQR 1.0–4.6 years).

Results Subjects were aged 77±13 years and 57.4% were female. Overall, 2049 (13.7%), 5085 (33.9%), 4380 (29.3%), 1956 (13.1%) and 1510 (10.1%) patients had no (eRVSP<30.00 mm Hg), borderline (30.00–39.99 mm Hg), mild (40.00–49.99 mm Hg), moderate (50.00–59.99 mm Hg) and severe PHT (>60.00 mm Hg), respectively. An echocardiographic phenotype was evident with worsening PHT, showing rising E:e’ ratio and right and left atrial sizes(p<0.0001, for all). Adjusted analyses showed that the risk of long-term mortality progressively rose as eRVSP level increased (HR 1.14–2.94, borderline to severe PHT, p<0.0001 for all). A mortality threshold was identified in the 4th decile of eRVSP categories (35.01–38.00 mm Hg; HR 1.19, 95% CI 1.04 to 1.35), with risk progressively increasing through to the 10th decile (HR 2.86, 95% CI 2.54 to 3.21).

Conclusions In this large cohort study, we find that PHT is common in ≥moderate AS and mortality increases as PHT becomes more severe. A threshold for higher mortality lies within the range of ‘borderline-mild’ PHT.

Trial registration number ACTRN12617001387314.

  • aortic valve stenosis
  • valvular heart disease
  • hypertension, pulmonary

Data availability statement

Data are available upon reasonable request. The NEDA collaboration encourages use of the NEDA data with the cooperation of participating sites and responsible NEDA investigators—a full list which is available (with contact details for advice on accessing data) via NEDA’s home website (https://www.neda.net.au/).

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Data availability statement

Data are available upon reasonable request. The NEDA collaboration encourages use of the NEDA data with the cooperation of participating sites and responsible NEDA investigators—a full list which is available (with contact details for advice on accessing data) via NEDA’s home website (https://www.neda.net.au/).

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Footnotes

  • Twitter @PlayfordDavid

  • Contributors SR and DSC conceived this analysis and conducted study analyses, and all authors contributed to the interpretation of study data. SR wrote the manuscript and all authors contributed to its revision. GS and DP conceived and designed the National Echo Database of Australia Study. GS and DP are the guarantors of the overall veracity and accuracy of NEDA data presented in this manuscript.

  • Funding This research did not receive any specific grants from funding agencies in the public, commercial, or not for profit sectors. However, NEDA has received investigator initiated funding support from Janssen, Novartis Pharmaceuticals and Edwards Lifesciences in the past 3 years. SR is supported by the Heart Research Institute Australia, Emerging Cardiovascular Researcher Education Scholarship. Both NEDA (grant 1055214) and SS (grant 11358940) are supported by the National Health and Medical Research Council of Australia.

  • Competing interests SS, DP and GS have previously received consultancy/speaking fees from Edwards LifeSciences. DP and GS have received consultancy fees from Medtronic, Edwards LifeSciences, Abbott Laboratories and ECHO IQ Pty Ltd. DSC is on the Editorial Board of BMJ HEART.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • © Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and permissions. Published by BMJ.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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