Sang-Eun Lee1,2, Ji Min Sung1,2, Daniele Andreini3, Matthew J Budoff4, Filippo Cademartiri5, Kavitha Chinnaiyan6, Jung Hyun Choi7, Eun Ju Chun8, Edoardo Conte3, Ilan Gottlieb9, Martin Hadamitzky10, Yong Jin Kim11, Amit Kumar12, Byoung Kwon Lee13, Jonathon A Leipsic14, Erica Maffei15, Hugo Marques16, Gianluca Pontone3, Gilbert Raff6, Sanghoon Shin17, Peter H Stone18, Habib Samady19, Renu Virmani20, Jagat Narula21, Daniel S Berman22, Leslee J Shaw19, Jeroen J Bax23, Fay Y Lin12, James K Min12, Hyuk-Jae Chang1,2. 1. Division of Cardiology, Department of Internal Medicine, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea. 2. Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Centre, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea. 3. Centro Cardiologico Monzino, IRCCS, Milan, Italy. 4. Department of Medicine, Los Angeles Biomedical Research Institute, Torrance, CA, USA. 5. Cardiovascular Imaging Unit, SDN Foundation IRCCS, Naples, Italy. 6. Department of Cardiology, William Beaumont Hospital, Royal Oak, MI, USA. 7. Department of Internal Medicine, Busan University Hospital, Busan, South Korea. 8. Department of Radiology, Seoul National University Bundang Hospital, Gyeonggi-do, South Korea. 9. Department of Radiology, Casa de Saude São Jose, Rio de Janeiro, Brazil. 10. Department of Radiology and Nuclear Medicine, German Heart Centre Munich, Munich, Germany. 11. Department of Internal Medicine, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, South Korea. 12. Dalio Institute of Cardiovascular Imaging, New York-Presbyterian Hospital and Weill Cornell Medical College, New York, NY, USA. 13. Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. 14. Department of Medicine and Radiology, University of British Columbia, Vancouver, BC, Canada. 15. Department of Radiology, Area Vasta 1/ASUR Marche, Urbino, Italy. 16. UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisbon, Portugal. 17. Department of Internal Medicine, National Health Insurance Service Ilsan Hospital, Gyeonggi-do, South Korea. 18. Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA, USA. 19. Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA. 20. Department of Pathology, CVPath Institute, Gaithersburg, MD, USA. 21. Icahn School of Medicine at Mount Sinai, Mount Sinai Heart, Zena and Michael A. Wiener Cardiovascular Institute, and Marie-Josee and Henry R. Kravis Centre for Cardiovascular Health, New York, NY, USA. 22. Department of Imaging and Medicine, Cedars-Sinai Medical Centre, Los Angeles, CA, USA. 23. Department of Cardiology, Leiden University Medical Centre, ZA Leiden, The Netherlands.
Abstract
AIMS: Coronary artery calcium score (CACS) is a strong predictor of major adverse cardiac events (MACE). Conversely, statins, which markedly reduce MACE risk, increase CACS. We explored whether CACS progression represents compositional plaque volume (PV) progression differently according to statin use. METHODS AND RESULTS: From a prospective multinational registry of consecutive patients (n = 2252) who underwent serial coronary computed tomography angiography (CCTA) at a ≥ 2-year interval, 654 patients (61 ± 10 years, 56% men, inter-scan interval 3.9 ± 1.5 years) with information regarding the use of statins and having a serial CACS were included. Patients were divided into non-statin (n = 246) and statin-taking (n = 408) groups. Coronary PVs (total, calcified, and non-calcified; sum of fibrous, fibro-fatty, and lipid-rich) were quantitatively analysed, and CACS was measured from both CCTAs. Multivariate linear regression models were constructed for both statin-taking and non-statin group to assess the association between compositional PV change and change in CACS. In multivariate linear regression analysis, in the non-statin group, CACS increase was positively associated with both non-calcified (β = 0.369, P = 0.004) and calcified PV increase (β = 1.579, P < 0.001). However, in the statin-taking group, CACS increase was positively associated with calcified PV change (β = 0.756, P < 0.001) but was negatively associated with non-calcified PV change (β = -0.194, P = 0.026). CONCLUSION: In the non-statin group, CACS progression indicates the progression of both non-calcified and calcified PV progression. However, under the effect of statins, CACS progression indicates only calcified PV progression, but not non-calcified PV progression. Thus, the result of serial CACS should be differently interpreted according to the use of statins. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: Coronary artery calcium score (CACS) is a strong predictor of major adverse cardiac events (MACE). Conversely, statins, which markedly reduce MACE risk, increase CACS. We explored whether CACS progression represents compositional plaque volume (PV) progression differently according to statin use. METHODS AND RESULTS: From a prospective multinational registry of consecutive patients (n = 2252) who underwent serial coronary computed tomography angiography (CCTA) at a ≥ 2-year interval, 654 patients (61 ± 10 years, 56% men, inter-scan interval 3.9 ± 1.5 years) with information regarding the use of statins and having a serial CACS were included. Patients were divided into non-statin (n = 246) and statin-taking (n = 408) groups. Coronary PVs (total, calcified, and non-calcified; sum of fibrous, fibro-fatty, and lipid-rich) were quantitatively analysed, and CACS was measured from both CCTAs. Multivariate linear regression models were constructed for both statin-taking and non-statin group to assess the association between compositional PV change and change in CACS. In multivariate linear regression analysis, in the non-statin group, CACS increase was positively associated with both non-calcified (β = 0.369, P = 0.004) and calcified PV increase (β = 1.579, P < 0.001). However, in the statin-taking group, CACS increase was positively associated with calcified PV change (β = 0.756, P < 0.001) but was negatively associated with non-calcified PV change (β = -0.194, P = 0.026). CONCLUSION: In the non-statin group, CACS progression indicates the progression of both non-calcified and calcified PV progression. However, under the effect of statins, CACS progression indicates only calcified PV progression, but not non-calcified PV progression. Thus, the result of serial CACS should be differently interpreted according to the use of statins. Published on behalf of the European Society of Cardiology. All rights reserved.
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