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Original research
Predictors of outcome in patients with moderate mixed aortic valve disease
  1. Kush P Patel1,2,
  2. Michael McKenna2,
  3. George D Thornton1,2,
  4. Sebastian Vandermolen1,3,
  5. Zaid Ali Abdulelah2,
  6. Wael Awad2,
  7. Andreas Baumbach2,3,
  8. Anthony Mathur2,3,
  9. Thomas A Treibel1,2,
  10. Guy Lloyd2,
  11. Michael J Mullen2,
  12. Sanjeev Bhattacharyya2
  1. 1 Institute of Cardiovascular Science, University College London, London, UK
  2. 2 Barts Heart Centre, West Smithfield, London, UK
  3. 3 The William Harvey Research Institute, Queen Mary University, London, UK
  1. Correspondence to Dr Sanjeev Bhattacharyya, Barts Heart Centre, St Bartholomew's Hospital, London EC1A 7BE, UK; Sanjeev.Bhattacharyya{at}


Objectives Grading the severity of moderate mixed aortic stenosis and regurgitation (MAVD) is challenging and the disease poorly understood. Identifying markers of haemodynamic severity will improve risk stratification and potentially guide timely treatment. This study aims to identify prognostic haemodynamic markers in patients with moderate MAVD.

Methods Moderate MAVD was defined as coexisting moderate aortic stenosis (aortic valve area (AVA) 1.0–1.5 cm2) and moderate aortic regurgitation (vena contracta (VC) 0.3–0.6 cm). Consecutive patients diagnosed between 2015 and 2019 were included from a multicentre registry. The primary composite outcome of death or heart failure hospitalisation was evaluated among these patients. Demographics, comorbidities, echocardiography and treatment data were assessed for their prognostic significance.

Results 207 patients with moderate MAVD were included, aged 78 (66–84) years, 56% male sex, AVA 1.2 (1.1–1.4) cm2 and VC 0.4 (0.4–0.5) cm. Over a follow-up of 3.5 (2.5–4.7) years, the composite outcome was met in 89 patients (43%). Univariable associations with the primary outcome included older age, previous myocardial infarction, previous cerebrovascular event, atrial fibrillation, New York Heart Association >2, worse renal function, tricuspid regurgitation ≥2 and mitral regurgitation ≥2. Markers of biventricular systolic function, cardiac remodelling and transaortic valve haemodynamics demonstrated an inverse association with the primary composite outcome. In multivariable analysis, peak aortic jet velocity (Vmax) was independently and inversely associated with the composite outcome (HR: 0.63, 95% CI 0.43 to 0.93; p=0.021) in an adjusted model along with age (HR: 1.05, 95% CI 1.03 to 1.08; p<0.001), creatinine (HR: 1.002, 95% CI 1.001 to 1.003; p=0.005), previous cerebrovascular event (85% vs 42%; HR: 3.04, 95% CI 1.54 to 5.99; p=0.001) and left ventricular ejection fraction (LVEF) (HR: 0.97, 95% CI 0.95 to 0.99; p=0.007). Patients with Vmax ≤2.8 m/s and LVEF ≤50% (n=27) had the worst outcome compared with the rest of the population (72% vs 41%; HR: 3.87, 95% CI 2.20 to 6.80; p<0.001).

Conclusions Patients with truly moderate MAVD have a high incidence of death and heart failure hospitalisation (43% at 3.5 (2.5–4.7) years). Within this group, a high-risk group characterised by disproportionately low aortic Vmax (≤2.8 m/s) and adverse remodelling (LVEF ≤50%) have the worst outcomes.

  • Echocardiography
  • Heart Valve Prosthesis Implantation
  • Transcatheter Aortic Valve Replacement
  • Aortic Valve Insufficiency
  • Aortic Valve Stenosis

Data availability statement

No data are available. Data for this study are not available due to confidentiality reasons.

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Data availability statement

No data are available. Data for this study are not available due to confidentiality reasons.

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  • KPP and MM are joint first authors.

  • X @ZaidHasanii

  • Contributors Conception and design: KPP, MM, SB, SV, GDT, AB. Data collection: all authors. Data analysis/interpretation: KPP, MM, SB, SV, GDT. Guaranter for data/analysis: KPP, MM, GT, SB. Drafting of the manuscript: KPP, MM, SB. Critical revision of the manuscript: all authors. Final approval of the manuscript: all authors. All authors agree to be accountable for all aspects of this manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests KPP has an unrestricted research grant from Edwards Lifesciences. TAT is directly and indirectly supported by the UCLH and Barts NIHR Biomedical Research Units. MJM has received grants and personal fees from Edwards Lifesciences and personal fees from Abbott Vascular.

  • 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.