Vulnerable plaques and patients: state-of-the-art

Author:

Tomaniak Mariusz12ORCID,Katagiri Yuki3,Modolo Rodrigo34ORCID,de Silva Ranil56,Khamis Ramzi Y5,Bourantas Christos V789,Torii Ryo10ORCID,Wentzel Jolanda J11,Gijsen Frank J H12,van Soest Gijs11ORCID,Stone Peter H13,West Nick E J14,Maehara Akiko1516,Lerman Amir17ORCID,van der Steen Antonius F W111819ORCID,Lüscher Thomas F2021,Virmani Renu22,Koenig Wolfgang232425,Stone Gregg W1516,Muller James E13ORCID,Wijns William2627,Serruys Patrick W528ORCID,Onuma Yoshinobu28

Affiliation:

1. Department of Cardiology, Erasmus Medical Centre, Thorax Centre, Rotterdam, The Netherlands

2. First Department of Cardiology, Medical University of Warsaw, Warsaw, Poland

3. Department of Clinical and Experimental Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands

4. Cardiology Division, Department of Internal Medicine, University of Campinas (UNICAMP), Campinas, Brazil

5. National Heart and Lung Institute, Imperial College London, London, UK

6. NIHR Cardiovascular Biomedical Research Unit, Institute of Cardiovascular Medicine and Science, Royal Brompton and Harefield NHS Foundation Trust, London, UK

7. Department of Cardiology, Barts Heart Centre, Barts Health NHS Trust, London EC1A 7BE, UK

8. William Harvey Research Institute, Queen Mary University London, Charterhouse Square, London EC1M 6BQ, UK

9. Institute of Cardiovascular Sciences, University College London, 62 Huntley St, Fitzrovia, London WC1E 6DD, UK

10. Department of Mechanical Engineering, University College London, Torrington Place, London WC1E 7JE, UK

11. Department of Cardiology, Biomedical Engineering, Erasmus Medical Centre, Rotterdam, The Netherlands

12. Department of Biomedical Engineering, Erasmus Medical Centre, Thorax Centre, Rotterdam, The Netherlands

13. Division of Cardiovascular Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA

14. Department of Interventional Cardiology, Royal Papworth Hospital, Papworth Rd, Trumpington, Cambridge CB2 0AY, UK

15. Division of Cardiology, New York-Presbyterian Hospital, Columbia University Medical Center, New York, NY, USA

16. Clinical Trials Centre, Cardiovascular Research Foundation, New York, NY, USA

17. Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA

18. Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China

19. Department of Imaging Physics, Faculty of Applied Sciences, Delft University of Technology, Delft, The Netherlands

20. Royal Brompton and Harefield Hospital Trust, Imperial College London, , London, UK

21. Centre for Molecular Cardiology, University of Zurich, Zurich, Switzerland

22. CVPath Institute, Gaithersburg, MD 20878, USA

23. Klinik für Herz- und Kreislauferkrankungen, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany

24. DZHK (German Centre for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany

25. Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany

26. The Lambe Institute for Translational Medicine and Curam, National University of Ireland, Galway, Ireland

27. Saolta University Healthcare Group, Galway, Ireland

28. Department of Cardiology, National University of Ireland, Galway, Ireland

Abstract

Abstract Despite advanced understanding of the biology of atherosclerosis, coronary heart disease remains the leading cause of death worldwide. Progress has been challenging as half of the individuals who suffer sudden cardiac death do not experience premonitory symptoms. Furthermore, it is well-recognized that also a plaque that does not cause a haemodynamically significant stenosis can trigger a sudden cardiac event, yet the majority of ruptured or eroded plaques remain clinically silent. In the past 30 years since the term ‘vulnerable plaque’ was introduced, there have been major advances in the understanding of plaque pathogenesis and pathophysiology, shifting from pursuing features of ‘vulnerability’ of a specific lesion to the more comprehensive goal of identifying patient ‘cardiovascular vulnerability’. It has been also recognized that aside a thin-capped, lipid-rich plaque associated with plaque rupture, acute coronary syndromes (ACS) are also caused by plaque erosion underlying between 25% and 60% of ACS nowadays, by calcified nodule or by functional coronary alterations. While there have been advances in preventive strategies and in pharmacotherapy, with improved agents to reduce cholesterol, thrombosis, and inflammation, events continue to occur in patients receiving optimal medical treatment. Although at present the positive predictive value of imaging precursors of the culprit plaques remains too low for clinical relevance, improving coronary plaque imaging may be instrumental in guiding pharmacotherapy intensity and could facilitate optimal allocation of novel, more aggressive, and costly treatment strategies. Recent technical and diagnostic advances justify continuation of interdisciplinary research efforts to improve cardiovascular prognosis by both systemic and ‘local’ diagnostics and therapies. The present state-of-the-art document aims to present and critically appraise the latest evidence, developments, and future perspectives in detection, prevention, and treatment of ‘high-risk’ plaques occurring in ‘vulnerable’ patients.

Funder

European Society of Cardiology

ESC

NIH

Publisher

Oxford University Press (OUP)

Subject

Cardiology and Cardiovascular Medicine

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