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Valvular heart disease
Original research
Prognostic implications of left ventricular diastolic dysfunction in moderate aortic stenosis
  1. Jan Stassen1,2,
  2. See Hooi Ewe3,
  3. Steele C Butcher1,
  4. Mohammed R Amanullah3,
  5. Bart J Mertens4,
  6. Kensuke Hirasawa1,
  7. Gurpreet K Singh1,
  8. Kenny Y Sin5,
  9. Zee Pin Ding3,
  10. Stephan M Pio1,
  11. Ching-Hui Sia6,
  12. Nicholas Chew6,
  13. William Kong6,
  14. Kian Keong Poh6,
  15. David Cohen7,
  16. Philippe Généreux8,
  17. Martin B Leon9,
  18. Nina Ajmone Marsan1,
  19. Victoria Delgado1,
  20. Jeroen J Bax1,10
  1. 1 Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands
  2. 2 Department of Cardiology, Jessa Hospital, Hasselt, Belgium
  3. 3 Department of Cardiology, National Heart Centre Singapore, Singapore
  4. 4 Department of Bioinformatics, Leiden University Medical Centre, Leiden, The Netherlands
  5. 5 Department of Cardiothoracic Surgery, National Heart Centre Singapore, Singapore
  6. 6 Department of Cardiology, National University Heart Centre, Singapore
  7. 7 Department of Cardiology, Saint Francis Hospital The Heart Center, Roslyn, New York, USA
  8. 8 Department of Cardiology, Morristown Medical Center, Morristown, New Jersey, USA
  9. 9 Department of Cardiology, Columbia University Medical Center, New York, New York, USA
  10. 10 Department of Cardiology, Turku Heart Center, Turku, Finland
  1. Correspondence to Professor Jeroen J Bax, Department of Cardiology, Leiden Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands; j.j.bax{at}lumc.nl

Abstract

Objective To investigate the prognostic impact of left ventricular (LV) diastolic dysfunction in patients with moderate aortic stenosis (AS) and preserved LV systolic function.

Methods Patients with a first diagnosis of moderate AS (aortic valve area >1.0 and ≤1.5 cm2) and preserved LV systolic function (LV ejection fraction ≥50%) were identified. LV diastolic function was evaluated using echocardiographic criteria according to the 2016 American Society of Echocardiography/European Association of Cardiovascular Imaging guidelines. Clinical outcomes were defined as all-cause mortality and a composite of all-cause mortality and aortic valve replacement (AVR).

Results Of 1247 patients (age 74±10 years, 47% men), 535 (43%) had LV diastolic dysfunction at baseline. Patients with LV diastolic dysfunction showed significantly higher mortality rates at 1-year, 3-year and 5-year follow-up (13%, 30% and 41%, respectively) when compared with patients with normal LV diastolic function (6%, 17% and 29%, respectively) (p<0.001). On multivariable analysis, LV diastolic dysfunction was independently associated with all-cause mortality (HR 1.368; 95% CI 1.085 to 1.725; p=0.008) and the composite endpoint of all-cause mortality and AVR (HR 1.241; 95% CI 1.035 to 1.488; p=0.020).

Conclusions LV diastolic dysfunction is independently associated with all-cause mortality and the composite endpoint of all-cause mortality and AVR in patients with moderate AS and preserved LV systolic function. Assessment of LV diastolic function therefore contributes significantly to the risk stratification of patients with moderate AS. Future clinical trials are needed to investigate whether patients with moderate AS and LV diastolic dysfunction may benefit from earlier valve intervention.

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

Data availability statement

Data are available upon reasonable request.

https://doi.org/10.1136/heartjnl-2022-320886

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    Data availability statement

    Data are available upon reasonable request.

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    Footnotes

    • Twitter @khircvm, @djc795

    • Contributors All authors contributed to the conception and design of the study. JS, SHE, SCB and KH analysed the data; all authors contributed to the interpretation of the data. Drafting of the manuscript was done by JS, SHE and JJB; the manuscript was critically revised by all authors. In addition, all authors gave final approval and agreed to be accountable for all aspects of the work. JJB is the guarantor.

    • Funding JS received funding from the European Society of Cardiology (ESC Training Grant App000064741). SCB received funding from the European Society of Cardiology (ESC Research Grant App000080404).

    • Competing interests The Department of Cardiology of the Leiden University Medical Centre received unrestricted research grants from Abbott Vascular, Bayer, Biotronik, Bioventrix, Boston Scientific, Edwards Lifesciences, GE Healthcare and Medtronic. JJB received speaker fees from Abbott Vascular. NAM received speaker fees from Abbott Vascular and GE Healthcare. VD received speaker fees from Abbott Vascular, Edwards Lifesciences, MSD and GE Healthcare. The remaining authors have nothing to disclose.

    • Patient and public involvement Patients and/or the public were involved in the design, or conduct, or reporting or dissemination plans of this research. Refer to the Methods section for further details.

    • 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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