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Pulmonary vascular disease
Original research
Prevalence of pulmonary hypertension in aortic regurgitation and its influence on outcomes
  1. Seshika Ratwatte1,2,
  2. David Playford3,
  3. Simon Stewart3,4,
  4. Geoff Strange5,6,
  5. David S Celermajer1,2
  1. 1 Department of Cardiology, Royal Prince Albert Hospital, Camperdown, New South Wales, Australia
  2. 2 Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia
  3. 3 Institute for Health Research, The University of Notre Dame Australia, Fremantle, Western Australia, Australia
  4. 4 School of Medicine, Dentistry and Nursing, University of Glasgow, Glasgow, UK
  5. 5 Heart Research Institute Ltd, Newtown, New South Wales, Australia
  6. 6 The University of Notre Dame Australia School of Medicine, Fremantle, Western Australia, 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 Aortic regurgitation (AR) can lead to pulmonary hypertension (PHT). There is a paucity of data on the prognostic importance of PHT in these patients. We therefore 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 AR were included (n=8392). These subjects were then categorised according to their eRVSP. The relationship between PHT severity and mortality outcomes were evaluated (median follow-up of 3.1 years, IQR 1.5–5.7 years).

Results Subjects were aged 74±14 years and 58.4% (4901) were female. Overall, 1417 (16.9%) had no PHT, and 3253 (38.8%), 2249 (26.9%), 893 (10.6%) and 580 (6.9%) patients had borderline, mild, moderate and severe PHT, respectively. Mean eRVSP was slightly higher in females than males (41±13 vs 39±12 mm Hg, p<0.0001) and increased with age in both sexes. After adjustment for age and sex, the risk of long-term mortality increased as eRVSP increased (adjusted HR (aHR) 1.20, 95% CI 1.06 to 1.36 in borderline PHT, to aHR 3.32, 95% CI 2.85 to 3.86 in severe PHT, p<0.0001). There was a mortality threshold seen from mild PHT onwards (eRVSP 41.36–44.15 mm Hg; aHR 1.41, 95%CI 1.17 to 1.68).

Conclusions In this large cohort study, we characterise the relationship between AR and PHT in adults. In patients with ≥moderate AR, PHT is associated with a progressive risk of mortality, even at mildly elevated levels.

  • Valvular Heart Disease
  • Hypertension, Pulmonary
  • Aortic Valve Insufficiency

Data availability statement

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

https://doi.org/10.1136/heartjnl-2022-322187

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    Data availability statement

    Data are available on reasonable request. Data are available on reasonable request. The National Echo Database of Australia (NEDA) collaboration encourages use of the NEDA data with the cooperation of participating sites and responsible NEDA investigators—a full list of 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 GS and DP conceived and designed the National Echo Database of Australia Study. SR and DSC conceived this analysis and conducted study analyses, and all authors contributed to the interpretation of study data. SR and DSC wrote the manuscript, and all authors contributed to its revision. 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.

    • 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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