Sang-Eun Lee1, Hyuk-Jae Chang2, Ji Min Sung1, Hyung-Bok Park3, Ran Heo4, Asim Rizvi5, Fay Y Lin5, Amit Kumar5, Martin Hadamitzky6, Yong Jin Kim7, Edoardo Conte8, Daniele Andreini8, Gianluca Pontone8, Matthew J Budoff9, Ilan Gottlieb10, Byoung Kwon Lee11, Eun Ju Chun12, Filippo Cademartiri13, Erica Maffei14, Hugo Marques15, Jonathon A Leipsic16, Sanghoon Shin17, Jung Hyun Choi18, Kavitha Chinnaiyan19, Gilbert Raff19, Renu Virmani20, Habib Samady21, Peter H Stone22, Daniel S Berman23, Jagat Narula24, Leslee J Shaw21, Jeroen J Bax25, James K Min5. 1. Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea; Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea. 2. Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea; Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea. Electronic address: hjchang@yuhs.ac. 3. Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea; Department of Internal Medicine, Division of Cardiology, Catholic Kwandong University International St. Mary's Hospital, Incheon, South Korea. 4. Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea; Division of Cardiology, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, South Korea. 5. Dalio Institute of Cardiovascular Imaging, New York-Presbyterian Hospital and Weill Cornell Medical College, New York, New York. 6. Department of Radiology and Nuclear Medicine, German Heart Center Munich, Munich, Germany. 7. Seoul National University College of Medicine, Seoul National University Hospital, South Korea. 8. Centro Cardiologico Monzino, IRCCS, Milan, Italy. 9. Department of Medicine, Los Angeles Biomedical Research Institute, Torrance, California. 10. Department of Radiology, Casa de Saude São Jose, Rio de Janeiro, Brazil. 11. Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. 12. Seoul National University Bundang Hospital, Seoul, South Korea. 13. Cardiovascular Imaging Center, SDN Foundation IRCCS, Naples, Italy. 14. Department of Radiology, Area Vasta 1/ASUR Marche, Urbino, Italy. 15. UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisbon, Portugal. 16. Department of Medicine and Radiology, University of British Columbia, Vancouver, British Columbia, Canada. 17. National Health Insurance Service Ilsan Hospital, Goyang, South Korea. 18. Busan University Hospital, Busan, South Korea. 19. Department of Cardiology, William Beaumont Hospital, Royal Oak, Michigan. 20. Department of Pathology, CVPath Institute, Gaithersburg, Maryland. 21. Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia. 22. Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, Massachusetts. 23. Department of Imaging and Medicine, Cedars-Sinai Medical Center, Los Angeles, California. 24. Icahn School of Medicine at Mount Sinai, Mount Sinai Heart, Zena and Michael A. Wiener Cardiovascular Institute, and Marie-Josée and Henry R. Kravis Center for Cardiovascular Health, New York, New York. 25. Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Abstract
OBJECTIVES: This study sought to describe the impact of statins on individual coronary atherosclerotic plaques. BACKGROUND: Although statins reduce the risk of major adverse cardiovascular events, their long-term effects on coronary atherosclerosis remain unclear. METHODS: We performed a prospective, multinational study consisting of a registry of consecutive patients without history of coronary artery disease who underwent serial coronary computed tomography angiography at an interscan interval of ≥2 years. Atherosclerotic plaques were quantitatively analyzed for percent diameter stenosis (%DS), percent atheroma volume (PAV), plaque composition, and presence of high-risk plaque (HRP), defined by the presence of ≥2 features of low-attenuation plaque, positive arterial remodeling, or spotty calcifications. RESULTS: Among 1,255 patients (60 ± 9 years of age; 57% men), 1,079 coronary artery lesions were evaluated in statin-naive patients (n = 474), and 2,496 coronary artery lesions were evaluated in statin-taking patients (n = 781). Compared with lesions in statin-naive patients, those in statin-taking patients displayed a slower rate of overall PAV progression (1.76 ± 2.40% per year vs. 2.04 ± 2.37% per year, respectively; p = 0.002) but more rapid progression of calcified PAV (1.27 ± 1.54% per year vs. 0.98 ± 1.27% per year, respectively; p < 0.001). Progression of noncalcified PAV and annual incidence of new HRP features were lower in lesions in statin-taking patients (0.49 ± 2.39% per year vs. 1.06 ± 2.42% per year and 0.9% per year vs. 1.6% per year, respectively; all p < 0.001). The rates of progression to >50% DS were not different (1.0% vs. 1.4%, respectively; p > 0.05). Statins were associated with a 21% reduction in annualized total PAV progression above the median and 35% reduction in HRP development. CONCLUSIONS: Statins were associated with slower progression of overall coronary atherosclerosis volume, with increased plaque calcification and reduction of high-risk plaque features. Statins did not affect the progression of percentage of stenosis severity of coronary artery lesions but induced phenotypic plaque transformation. (Progression of AtheRosclerotic PlAque DetermIned by Computed TomoGraphic Angiography Imaging [PARADIGM]; NCT02803411).
OBJECTIVES: This study sought to describe the impact of statins on individual coronary atherosclerotic plaques. BACKGROUND: Although statins reduce the risk of major adverse cardiovascular events, their long-term effects on coronary atherosclerosis remain unclear. METHODS: We performed a prospective, multinational study consisting of a registry of consecutive patients without history of coronary artery disease who underwent serial coronary computed tomography angiography at an interscan interval of ≥2 years. Atherosclerotic plaques were quantitatively analyzed for percent diameter stenosis (%DS), percent atheroma volume (PAV), plaque composition, and presence of high-risk plaque (HRP), defined by the presence of ≥2 features of low-attenuation plaque, positive arterial remodeling, or spotty calcifications. RESULTS: Among 1,255 patients (60 ± 9 years of age; 57% men), 1,079 coronary artery lesions were evaluated in statin-naive patients (n = 474), and 2,496 coronary artery lesions were evaluated in statin-taking patients (n = 781). Compared with lesions in statin-naive patients, those in statin-taking patients displayed a slower rate of overall PAV progression (1.76 ± 2.40% per year vs. 2.04 ± 2.37% per year, respectively; p = 0.002) but more rapid progression of calcified PAV (1.27 ± 1.54% per year vs. 0.98 ± 1.27% per year, respectively; p < 0.001). Progression of noncalcified PAV and annual incidence of new HRP features were lower in lesions in statin-taking patients (0.49 ± 2.39% per year vs. 1.06 ± 2.42% per year and 0.9% per year vs. 1.6% per year, respectively; all p < 0.001). The rates of progression to >50% DS were not different (1.0% vs. 1.4%, respectively; p > 0.05). Statins were associated with a 21% reduction in annualized total PAV progression above the median and 35% reduction in HRP development. CONCLUSIONS: Statins were associated with slower progression of overall coronary atherosclerosis volume, with increased plaque calcification and reduction of high-risk plaque features. Statins did not affect the progression of percentage of stenosis severity of coronary artery lesions but induced phenotypic plaque transformation. (Progression of AtheRosclerotic PlAque DetermIned by Computed TomoGraphic Angiography Imaging [PARADIGM]; NCT02803411).
Authors: Axel Schmermund; Joachim Eckert; Marco Schmidt; Annett Magedanz; Thomas Voigtländer Journal: Clin Res Cardiol Date: 2018-07-04 Impact factor: 5.460
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Authors: Stijn Devuyst; Arno Gigase; Jerrold Spapen; Sofie Brouwers; Thomas Couck; Jeroen Sonck; Takuya Mizukami; Carlo Gigante; Herbert de Raedt; Dan Schelfaut; Ward Heggermont; Bernard De Bruyne; Martin Penicka; Guy Van Camp; Carlos Collet Journal: Cardiovasc Diagn Ther Date: 2019-06