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Valvular heart disease
Original research
Aortic valve perivascular adipose tissue computed tomography attenuation in patients with aortic stenosis
  1. Simona B Botezatu1,2,
  2. Xinming Yu1,
  3. Mohammed N Meah1,
  4. Michelle C Williams1,
  5. Damini Dey3,
  6. David E Newby1,
  7. Evangelos Tzolos1,
  8. Marc R Dweck1
  1. 1 British Heart Foundation Centre for Cardiovascular Science, The University of Edinburgh, Edinburgh, UK
  2. 2 Cardiology Department, Euroecolab, University of Medicine and Pharmacy 'Carol Davila', Bucharest, Romania
  3. 3 Biomedical Imaging Research Institute, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California, USA
  1. Correspondence to Professor Marc R Dweck, Centre for Cardiovascular Science, The University of Edinburgh, Edinburgh EH16 4SB, UK; marc.dweck{at}ed.ac.uk

Abstract

Objective Aortic stenosis (AS) shares pathophysiological similarities with atherosclerosis including active inflammation. CT attenuation of perivascular adipose tissue provides a measure of vascular inflammation that is linked to prognosis and has the potential to be applied to the aortic valve. We investigated perivascular adipose tissue attenuation around the aortic valve in patients with AS.

Methods CT attenuation was measured in the perivascular adipose tissue extending 3 mm radially and 10 mm longitudinally around the aortic valve in patients with and without AS. Associations between perivascular adipose tissue attenuation and AS disease severity, activity and progression were investigated.

Results Perivascular adipose tissue attenuation around the aortic valve demonstrated good intraobserver and interobserver repeatability (interobserver: intraclass correlation coefficient 0.977 (95% CI: 0.94, 0.99)) but was similar between patients with AS (n=120) and control subjects (n=80) (−62.4 (−68.7, −56.5) Hounsfield units (HU) vs −61.2 (−65.3, −55.6) HU, p=0.099). There were no differences between perivascular adipose tissue attenuation in patients with mild (−60.2 (−66.9, −55.1) HU), moderate (−62.8 (−69.6, −56.80) HU) or severe (−62.3 (−69.3, −55.4) HU) AS (all p>0.05), and perivascular adipose tissue attenuation did not demonstrate an association with AS severity as assessed by echocardiography or CT calcium scoring, nor with disease activity assessed by 18F-sodium fluoride positron emission tomography. Moreover, there was no association between baseline aortic valve perivascular adipose tissue attenuation and subsequent AS progression (annualised change in peak velocity: r=0.072, p=0.458). Similar results were found using five other image analysis methods.

Conclusions CT-derived aortic valve perivascular adipose tissue attenuation is not associated with AS disease severity, activity or progression suggesting that it has no value in the investigation and management of patients with AS.

  • aortic stenosis
  • computed tomography angiography
  • heart valve diseases

Data availability statement

Data are available upon reasonable request. The data underlying this article will be shared on reasonable request to the corresponding author.

https://doi.org/10.1136/heartjnl-2023-323217

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    Data availability statement

    Data are available upon reasonable request. The data underlying this article will be shared on reasonable request to the corresponding author.

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    Footnotes

    • SBB and XY are joint first authors.

    • ET and MRD are joint senior authors.

    • X @imagingmedsci, @TzolosEvangelos

    • SBB and XY contributed equally.

    • ET and MRD contributed equally.

    • Presented at Parts of these results were presented at the The State-of-the-Art Cardiovascular CT meeting 2023 (Botezatu S, Yu X, Meah M, Dey D, Newby D, Tzolos E, Dweck M. Aortic Valve Perivascular Adipose Tissue Computed Tomography Attenuation And The Assessment Of Valve Inflammation In Patients With Aortic Stenosis. Journal of cardiovascular computed tomography 2023 Jan, Volume 17, Issue 1, Supplement S6–S7).

    • Contributors MRD is responsible for the overall content as guarantor. SBB and XY participated in the study design and analysis and interpretation of the final data, as well as in the drafting of the manuscript. MNM, MCW, DD and DEN made critical revisions of the paper. ET and MRD were responsible for the design and supervision of the study and approval of the final manuscript. SBB and XY contributed equally to this paper. ET and MRD contributed equally to this paper.

    • Funding SBB is supported by a Romanian Society of Cardiology Research Grant (contract no 266/8.06.2021). MCW is supported by the British Heart Foundation (FS/ICRF/20/26002). DEN is supported by the British Heart Foundation (CH/09/002, RE/18/5/34216, RG/F/22/110093). MRD is supported by the British Heart Foundation (FS/SCRF/21/32010) and is the recipient of the Sir Jules Thorn Award for Biomedical Research 2015 (15/JTA).

    • Competing interests None declared.

    • 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.