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Original research
Pericoronary adipose tissue density is increased in patients with recent spontaneous coronary dissection
  1. Rafał R Wolny1,
  2. Jacek Kwieciński1,
  3. Joanna Zalewska1,
  4. Ilona Michałowska2,
  5. Mariusz Kruk3,
  6. Cezary Kepka3,
  7. Aleksander Prejbisz4,
  8. Jerzy Pręgowski1,
  9. Alicja Chwała1,
  10. Jarosław Skowroński1,
  11. Agata Kobierska5,
  12. Radosław Ciesielski5,
  13. Andrzej Januszewicz6,
  14. Adam Witkowski1,
  15. David Adlam7,
  16. Damini Dey8,
  17. Jacek Kądziela1
  1. 1 Department of Interventional Cardiology and Angiology, National Institute of Cardiology, Warsaw, Poland
  2. 2 Department of Radiology, National Institute of Cardiology, Warsaw, Poland
  3. 3 Department of Coronary and Structural Heart Diseases, National Institute of Cardiology, Warsaw, Poland
  4. 4 Department of Epidemiology, Cardiovascular Disease Prevention and Health Promotion, National Institute of Cardiology, Warsaw, Poland
  5. 5 Medical University of Warsaw, Warsaw, Poland
  6. 6 Department of Hypertension, National Institute of Cardiology, Warsaw, Poland
  7. 7 Department of Cardiovascular Sciences, University of Leicester, Leicester, UK
  8. 8 Biomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA
  1. Correspondence to Dr Rafał R Wolny, Department of Interventional Cardiology and Angiology, National Institute of Cardiology, Warsaw, Poland; rwolny{at}ikard.pl

Abstract

Objective Inflammatory activity is one of the potential mechanisms of spontaneous coronary artery dissection (SCAD). Recently, the pericoronary adipose tissue attenuation (PCAT) derived from CT angiography (CTA) has been established as a method for measuring vascular inflammation. We aimed to characterise the pancoronary and vessel-specific PCAT in patients with and without recent SCAD.

Methods The study comprised patients with SCAD referred to a tertiary centre between 2017 and 2022 who underwent CTA and were compared with individuals with no prior SCAD. PCAT was analysed on end-diastolic CTA reconstructions along proximal 40 mm of all major coronary vessels as well as the SCAD-related vessel. We analysed 48 patients with recent SCAD (median 6.1 (IQR 3.5–14.9) months since SCAD, 95.8% female) and 48 patients in the group without SCAD.

Results Pancoronary PCAT was higher in patients with SCAD compared with those without SCAD (−80.6±7.9 vs −85.3 HU±6.1, p=0.002). Vessel-specific PCAT in patients with SCAD compared with patients without SCAD was higher for both the RCA (−80.9±9.5 vs −87.1±6.9 HU, p=0.001) and the LCA (−80.3±7.8 vs −83.4±7.2 HU, p=0.04). In patients with SCAD, PCAT of the SCAD-related vessel was not significantly different from averaged PCAT of unaffected vessels (−81.2±9.2 vs −80.6±7.6, p=0.74). There was no association between PCAT and the interval from SCAD to CTA.

Conclusions Patients with recent SCAD have higher PCAT compared with patients without SCAD, suggesting an increased perivascular inflammatory activity. This association is not restricted to the dissected vessel.

  • Inflammation
  • Computed Tomography Angiography

Data availability statement

Data are available upon reasonable request.

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Data availability statement

Data are available upon reasonable request.

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Footnotes

  • Twitter @RafalWolny, @radcie98

  • Contributors RRW, JKw, JKą, AJ, DA and AP: conceptualisation of the study; JKą, JZ, AK and RC: coordination of the Polish SCAD registry; RRW, AC, JZ, JPr and JS: data gathering and analysis; RRW, JKw, JKą and AC: PCAT and angiography analysis; IM, MK and CK: performing all CTA scans; DA, AW and DD: revisions and advisory role; all authors: editing and proofreading of the manuscript. RRW is the guarantor.

  • Funding RRW and AC were supported by the Polish National Science Centre (grant number 2021/43/D/NZ5/02434). JKw was also supported by the Polish National Science Centre (grant number 2021/41/B/NZ5/02630).

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, conduct, 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.