Sang-Eun Lee1, Ji Min Sung2, Daniele Andreini3, Mouaz H Al-Mallah4, Matthew J Budoff5, Filippo Cademartiri6, Kavitha Chinnaiyan7, Jung Hyun Choi8, Eun Ju Chun9, Edoardo Conte3, Ilan Gottlieb10, Martin Hadamitzky11, Yong Jin Kim12, Byoung Kwon Lee13, Jonathon A Leipsic14, Erica Maffei15, Hugo Marques16, Pedro de Araújo Gonçalves16, Gianluca Pontone3, Gilbert L Raff7, Sanghoon Shin17, Peter H Stone18, Habib Samady19, Renu Virmani20, Jagat Narula21, Daniel S Berman22, Leslee J Shaw23, Jeroen J Bax24, Fay Y Lin23, James K Min23, Hyuk-Jae Chang25. 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; Division of Cardiology, Department of Internal Medicine, Ewha Womans University Seoul Hospital, 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. 3. Centro Cardiologico Monzino, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, Italy. 4. Houston Methodist DeBakey Heart & Vascular Center, Houston Methodist Hospital, Houston, Texas. 5. Department of Medicine, Los Angeles Biomedical Research Institute, Torrance, California. 6. Cardiovascular Imaging Unit, SDN IRCCS, Naples, Italy. 7. Department of Cardiology, William Beaumont Hospital, Royal Oak, Minnesota. 8. Pusan University Hospital, Busan, South Korea. 9. Seoul National University Bundang Hospital, Seongnam, South Korea. 10. Department of Radiology, Casa de Saude São Jose, Rio de Janeiro, Brazil. 11. Department of Radiology and Nuclear Medicine, German Heart Center Munich, Munich, Germany. 12. Department of Internal Medicine, Seoul National University College of Medicine, Cardiovascular Center, Seoul National University Hospital, Seoul, South Korea. 13. Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. 14. Department of Medicine and Radiology, University of British Columbia, Vancouver, British Columbia, Canada. 15. Department of Radiology, Area Vasta 1/ Azienda Sanitaria Unica Regionale (ASUR) Marche, Urbino, Italy. 16. UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisbon, Portugal. 17. Division of Cardiology, Department of Internal Medicine, Ewha Womans University Seoul Hospital, Seoul, South Korea. 18. Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, Massachusetts. 19. Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia. 20. Department of Pathology, CVPath Institute, Gaithersburg, Maryland. 21. Icahn School of Medicine at Mount Sinai, New York, New York. 22. Department of Imaging and Medicine, Cedars-Sinai Medical Center, Los Angeles, California. 23. Department of Radiology, New York-Presbyterian Hospital and Weill Cornell Medicine, New York, New York. 24. Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands. 25. 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.
Abstract
OBJECTIVES: This study explored whether the pattern of nonobstructive lesion progression into obstructive lesions would differ according to the presence of high-risk plaque (HRP). BACKGROUND: It is still debatable whether HRP simply represents a certain phase during the natural history of coronary atherosclerotic plaques or if disease progression would differ according to the presence of HRP. METHODS: Patients with nonobstructive coronary artery disease, defined as percent diameter stenosis (%DS) <50%, were enrolled from a prospective, multinational registry of consecutive patients who underwent serial coronary computed tomography angiography at an interscan interval of ≥2 years. HRP was defined as lesions with ≥2 features of positive remodeling, spotty calcification, or low-attenuation plaque. Quantitative total and compositional percent atheroma volume (PAV) at baseline and annualized PAV change were compared between non-HRP and HRP lesions. RESULTS: A total of 3,049 nonobstructive lesions were identified from 1,297 patients (mean age 60.3 ± 9.3 years; 56.8% men). There were 2,624 non-HRP and 425 HRP lesions. HRP lesions had a greater total PAV and all noncalcified components of PAV and %DS at baseline compared with non-HRP lesions. However, the annualized total PAV changes were greater in non-HRP lesions than in HRP lesions. On multivariate analysis adjusted for clinical risk factors, drug use, change in lipid level, total PAV, %DS, and HRP, only the baseline total PAV and %DS independently predicted the development of obstructive lesions (hazard ratio [HR]: 1.04; 95% confidence interval [CI]: 1.02 to 1.07, and HR: 1.07; 95% CI: 1.04 to 1.10, respectively, all p < 0.05), whereas the presence of HRP did not (p > 0.05). CONCLUSIONS: The pattern of individual coronary atherosclerotic plaque progression differed according to the presence of HRP. Baseline PAV, not the presence of HRP features, was the most important predictor of lesions developing into obstructive lesions. (Progression of Atherosclerotic Plaque Determined By Computed Tomographic Angiography Imaging [PARADIGM]; NCT02803411).
OBJECTIVES: This study explored whether the pattern of nonobstructive lesion progression into obstructive lesions would differ according to the presence of high-risk plaque (HRP). BACKGROUND: It is still debatable whether HRP simply represents a certain phase during the natural history of coronary atherosclerotic plaques or if disease progression would differ according to the presence of HRP. METHODS:Patients with nonobstructive coronary artery disease, defined as percent diameter stenosis (%DS) <50%, were enrolled from a prospective, multinational registry of consecutive patients who underwent serial coronary computed tomography angiography at an interscan interval of ≥2 years. HRP was defined as lesions with ≥2 features of positive remodeling, spottycalcification, or low-attenuation plaque. Quantitative total and compositional percent atheroma volume (PAV) at baseline and annualized PAV change were compared between non-HRP and HRP lesions. RESULTS: A total of 3,049 nonobstructive lesions were identified from 1,297 patients (mean age 60.3 ± 9.3 years; 56.8% men). There were 2,624 non-HRP and 425 HRP lesions. HRP lesions had a greater total PAV and all noncalcified components of PAV and %DS at baseline compared with non-HRP lesions. However, the annualized total PAV changes were greater in non-HRP lesions than in HRP lesions. On multivariate analysis adjusted for clinical risk factors, drug use, change in lipid level, total PAV, %DS, and HRP, only the baseline total PAV and %DS independently predicted the development of obstructive lesions (hazard ratio [HR]: 1.04; 95% confidence interval [CI]: 1.02 to 1.07, and HR: 1.07; 95% CI: 1.04 to 1.10, respectively, all p < 0.05), whereas the presence of HRP did not (p > 0.05). CONCLUSIONS: The pattern of individual coronary atherosclerotic plaque progression differed according to the presence of HRP. Baseline PAV, not the presence of HRP features, was the most important predictor of lesions developing into obstructive lesions. (Progression of Atherosclerotic Plaque Determined By Computed Tomographic Angiography Imaging [PARADIGM]; NCT02803411).
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