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Effects of Statins on Coronary Atherosclerotic Plaques: The PARADIGM Study.
JACC Cardiovasc Imaging. 2018 10; 11(10):1475-1484.JC

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).

Authors+Show Affiliations

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.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.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.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.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.Dalio Institute of Cardiovascular Imaging, New York-Presbyterian Hospital and Weill Cornell Medical College, New York, New York.Dalio Institute of Cardiovascular Imaging, New York-Presbyterian Hospital and Weill Cornell Medical College, New York, New York.Dalio Institute of Cardiovascular Imaging, New York-Presbyterian Hospital and Weill Cornell Medical College, New York, New York.Department of Radiology and Nuclear Medicine, German Heart Center Munich, Munich, Germany.Seoul National University College of Medicine, Seoul National University Hospital, South Korea.Centro Cardiologico Monzino, IRCCS, Milan, Italy.Centro Cardiologico Monzino, IRCCS, Milan, Italy.Centro Cardiologico Monzino, IRCCS, Milan, Italy.Department of Medicine, Los Angeles Biomedical Research Institute, Torrance, California.Department of Radiology, Casa de Saude São Jose, Rio de Janeiro, Brazil.Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.Seoul National University Bundang Hospital, Seoul, South Korea.Cardiovascular Imaging Center, SDN Foundation IRCCS, Naples, Italy.Department of Radiology, Area Vasta 1/ASUR Marche, Urbino, Italy.UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisbon, Portugal.Department of Medicine and Radiology, University of British Columbia, Vancouver, British Columbia, Canada.National Health Insurance Service Ilsan Hospital, Goyang, South Korea.Busan University Hospital, Busan, South Korea.Department of Cardiology, William Beaumont Hospital, Royal Oak, Michigan.Department of Cardiology, William Beaumont Hospital, Royal Oak, Michigan.Department of Pathology, CVPath Institute, Gaithersburg, Maryland.Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia.Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, Massachusetts.Department of Imaging and Medicine, Cedars-Sinai Medical Center, Los Angeles, California.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.Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia.Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.Dalio Institute of Cardiovascular Imaging, New York-Presbyterian Hospital and Weill Cornell Medical College, New York, New York.

Pub Type(s)

Journal Article
Multicenter Study
Observational Study
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29909109

Citation

Lee, Sang-Eun, et al. "Effects of Statins On Coronary Atherosclerotic Plaques: the PARADIGM Study." JACC. Cardiovascular Imaging, vol. 11, no. 10, 2018, pp. 1475-1484.
Lee SE, Chang HJ, Sung JM, et al. Effects of Statins on Coronary Atherosclerotic Plaques: The PARADIGM Study. JACC Cardiovasc Imaging. 2018;11(10):1475-1484.
Lee, S. E., Chang, H. J., Sung, J. M., Park, H. B., Heo, R., Rizvi, A., Lin, F. Y., Kumar, A., Hadamitzky, M., Kim, Y. J., Conte, E., Andreini, D., Pontone, G., Budoff, M. J., Gottlieb, I., Lee, B. K., Chun, E. J., Cademartiri, F., Maffei, E., ... Min, J. K. (2018). Effects of Statins on Coronary Atherosclerotic Plaques: The PARADIGM Study. JACC. Cardiovascular Imaging, 11(10), 1475-1484. https://doi.org/10.1016/j.jcmg.2018.04.015
Lee SE, et al. Effects of Statins On Coronary Atherosclerotic Plaques: the PARADIGM Study. JACC Cardiovasc Imaging. 2018;11(10):1475-1484. PubMed PMID: 29909109.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of Statins on Coronary Atherosclerotic Plaques: The PARADIGM Study. AU - Lee,Sang-Eun, AU - Chang,Hyuk-Jae, AU - Sung,Ji Min, AU - Park,Hyung-Bok, AU - Heo,Ran, AU - Rizvi,Asim, AU - Lin,Fay Y, AU - Kumar,Amit, AU - Hadamitzky,Martin, AU - Kim,Yong Jin, AU - Conte,Edoardo, AU - Andreini,Daniele, AU - Pontone,Gianluca, AU - Budoff,Matthew J, AU - Gottlieb,Ilan, AU - Lee,Byoung Kwon, AU - Chun,Eun Ju, AU - Cademartiri,Filippo, AU - Maffei,Erica, AU - Marques,Hugo, AU - Leipsic,Jonathon A, AU - Shin,Sanghoon, AU - Choi,Jung Hyun, AU - Chinnaiyan,Kavitha, AU - Raff,Gilbert, AU - Virmani,Renu, AU - Samady,Habib, AU - Stone,Peter H, AU - Berman,Daniel S, AU - Narula,Jagat, AU - Shaw,Leslee J, AU - Bax,Jeroen J, AU - Min,James K, Y1 - 2018/06/13/ PY - 2018/03/23/received PY - 2018/04/13/revised PY - 2018/04/16/accepted PY - 2018/6/18/pubmed PY - 2019/11/21/medline PY - 2018/6/18/entrez KW - coronary artery atherosclerosis KW - coronary artery disease KW - coronary computed tomography angiography KW - statins SP - 1475 EP - 1484 JF - JACC. Cardiovascular imaging JO - JACC Cardiovasc Imaging VL - 11 IS - 10 N2 - 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). SN - 1876-7591 UR - https://www.unboundmedicine.com/medline/citation/29909109/Effects_of_Statins_on_Coronary_Atherosclerotic_Plaques:_The_PARADIGM_Study_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1936-878X(18)30373-5 DB - PRIME DP - Unbound Medicine ER -