Alexander R van Rosendael1,2, Inge J van den Hoogen1,2, Umberto Gianni1,3, Xiaoyue Ma4, Sara W Tantawy1, A Maxim Bax1,2, Yao Lu4, Daniele Andreini5, Mouaz H Al-Mallah6, Matthew J Budoff7, Filippo Cademartiri8, Kavitha Chinnaiyan9, Jung Hyun Choi10, Edoardo Conte8, Hugo Marques11, Pedro de Araújo Gonçalves11, Ilan Gottlieb12, Martin Hadamitzky13, Jonathon A Leipsic14, Erica Maffei15, Gianluca Pontone5, Sanghoon Shin16, Yong-Jin Kim17, Byoung Kwon Lee18, Eun Ju Chun19, Ji Min Sung20,21, Sang-Eun Lee16,21, Renu Virmani22, Habib Samady23, Yu Sato22, Peter H Stone24, Daniel S Berman25, Jagat Narula26, Ron Blankstein24, James K Min27, Fay Y Lin1, Leslee J Shaw1, Jeroen J Bax2,28, Hyuk-Jae Chang20,29. 1. Department of Radiology, Dalio Institute of Cardiovascular Imaging, NewYork-Presbyterian Hospital and Weill Cornell Medicine, New York. 2. Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands. 3. Department of Molecular Medicine, Section of Cardiology, University of Pavia, Pavia, Italy. 4. Department of Healthcare Policy and Research, NewYork-Presbyterian Hospital and Weill Cornell Medical College, New York. 5. Centro Cardiologico Monzino, IRCCS Milan, Italy. 6. Houston Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital, Houston, Texas. 7. Department of Medicine, Los Angeles Biomedical Research Institute, Torrance, California. 8. Cardiovascular Imaging Center, SDN IRCCS, Naples, Italy. 9. Department of Cardiology, William Beaumont Hospital, Royal Oak, Michigan. 10. Pusan University Hospital, Busan, South Korea. 11. UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisboa, Portugal. 12. Department of Radiology, Casa de Saude São Jose, Rio de Janeiro, Brazil. 13. Department of Radiology and Nuclear Medicine, German Heart Center Munich, Munich, Germany. 14. Department of Medicine and Radiology, University of British Columbia, Vancouver, British Columbia, Canada. 15. Department of Radiology, Area Vasta 1/ASUR Marche, Urbino, Italy. 16. Division of Cardiology, Department of Internal Medicine, Ewha Woman's University Seoul Hospital, Seoul, Korea. 17. Department of Internal Medicine, Seoul National University College of Medicine, Cardiovascular Center, Seoul National University Hospital, Seoul, South Korea. 18. Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea. 19. Seoul National University Bundang Hospital, Sungnam, South Korea. 20. Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea. 21. Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea. 22. Department of Pathology, CVPath Institute, Gaithersburg, Maryland. 23. Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia. 24. Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. 25. Department of Imaging and Medicine, Cedars Sinai Medical Center, Los Angeles, California. 26. 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. 27. Cleerly Inc, New York, New York. 28. Heart Center, University of Turku and Turku University Hospital, Turku, Finland. 29. Ontact Health Inc, Seoul, South Korea.
Abstract
Importance: The density of atherosclerotic plaque forms the basis for categorizing calcified and noncalcified morphology of plaques. Objective: To assess whether alterations in plaque across a range of density measurements provide a more detailed understanding of atherosclerotic disease progression. Design, Setting, and Participants: This cohort study enrolled 857 patients who underwent serial coronary computed tomography angiography 2 or more years apart and had quantitative measurements of coronary plaques throughout the entire coronary artery tree. The study was conducted from 2013 to 2016 at 13 sites in 7 countries. Main Outcomes and Measures: The main outcome was progression of plaque composition of individual coronary plaques. Six plaque composition types were defined on a voxel-level basis according to the plaque attenuation (expressed in Hounsfield units [HU]): low attenuation (-30 to 75 HU), fibro-fatty (76-130 HU), fibrous (131-350 HU), low-density calcium (351-700 HU), high-density calcium (701-1000 HU), and 1K (>1000 HU). The progression rates of these 6 compositional plaque types were evaluated according to the interaction between statin use and baseline plaque volume, adjusted for risk factors and time interval between scans. Plaque progression was also examined based on baseline calcium density. Analysis was performed among lesions matched at baseline and follow-up. Data analyses were conducted from August 2019 through March 2020. Results: In total, 2458 coronary lesions in 857 patients (mean [SD] age, 62.1 [8.7] years; 540 [63.0%] men; 548 [63.9%] received statin therapy) were included. Untreated coronary lesions increased in volume over time for all 6 compositional types. Statin therapy was associated with volume decreases in low-attenuation plaque (β, -0.02; 95% CI, -0.03 to -0.01; P = .001) and fibro-fatty plaque (β, -0.03; 95% CI, -0.04 to -0.02; P < .001) and greater progression of high-density calcium plaque (β, 0.02; 95% CI, 0.01-0.03; P < .001) and 1K plaque (β, 0.02; 95% CI, 0.01-0.03; P < .001). When analyses were restricted to lesions without low-attenuation plaque or fibro-fatty plaque at baseline, statin therapy was not associated with a change in overall calcified plaque volume (β, -0.03; 95% CI, -0.08 to 0.02; P = .24) but was associated with a transformation toward more dense calcium. Interaction analysis between baseline plaque volume and calcium density showed that more dense coronary calcium was associated with less plaque progression. Conclusions and Relevance: The results suggest an association of statin use with greater rates of transformation of coronary atherosclerosis toward high-density calcium. A pattern of slower overall plaque progression was observed with increasing density. All findings support the concept of reduced atherosclerotic risk with increased densification of calcium.
Importance: The density of atherosclerotic plaque forms the basis for categorizing calcified and noncalcified morphology of plaques. Objective: To assess whether alterations in plaque across a range of density measurements provide a more detailed understanding of atherosclerotic disease progression. Design, Setting, and Participants: This cohort study enrolled 857 patients who underwent serial coronary computed tomography angiography 2 or more years apart and had quantitative measurements of coronary plaques throughout the entire coronary artery tree. The study was conducted from 2013 to 2016 at 13 sites in 7 countries. Main Outcomes and Measures: The main outcome was progression of plaque composition of individual coronary plaques. Six plaque composition types were defined on a voxel-level basis according to the plaque attenuation (expressed in Hounsfield units [HU]): low attenuation (-30 to 75 HU), fibro-fatty (76-130 HU), fibrous (131-350 HU), low-density calcium (351-700 HU), high-density calcium (701-1000 HU), and 1K (>1000 HU). The progression rates of these 6 compositional plaque types were evaluated according to the interaction between statin use and baseline plaque volume, adjusted for risk factors and time interval between scans. Plaque progression was also examined based on baseline calcium density. Analysis was performed among lesions matched at baseline and follow-up. Data analyses were conducted from August 2019 through March 2020. Results: In total, 2458 coronary lesions in 857 patients (mean [SD] age, 62.1 [8.7] years; 540 [63.0%] men; 548 [63.9%] received statin therapy) were included. Untreated coronary lesions increased in volume over time for all 6 compositional types. Statin therapy was associated with volume decreases in low-attenuation plaque (β, -0.02; 95% CI, -0.03 to -0.01; P = .001) and fibro-fatty plaque (β, -0.03; 95% CI, -0.04 to -0.02; P < .001) and greater progression of high-density calcium plaque (β, 0.02; 95% CI, 0.01-0.03; P < .001) and 1K plaque (β, 0.02; 95% CI, 0.01-0.03; P < .001). When analyses were restricted to lesions without low-attenuation plaque or fibro-fatty plaque at baseline, statin therapy was not associated with a change in overall calcified plaque volume (β, -0.03; 95% CI, -0.08 to 0.02; P = .24) but was associated with a transformation toward more dense calcium. Interaction analysis between baseline plaque volume and calcium density showed that more dense coronary calcium was associated with less plaque progression. Conclusions and Relevance: The results suggest an association of statin use with greater rates of transformation of coronary atherosclerosis toward high-density calcium. A pattern of slower overall plaque progression was observed with increasing density. All findings support the concept of reduced atherosclerotic risk with increased densification of calcium.
Authors: Gianluca Pontone; Alexia Rossi; Marco Guglielmo; Marc R Dweck; Oliver Gaemperli; Koen Nieman; Francesca Pugliese; Pal Maurovich-Horvat; Alessia Gimelli; Bernard Cosyns; Stephan Achenbach Journal: Eur Heart J Cardiovasc Imaging Date: 2022-03-22 Impact factor: 9.130
Authors: Emily Keyes; Madison Grinnell; Douglas Jacoby; Thomas Vazquez; DeAnna Diaz; Victoria P Werth; Kevin Jon Williams Journal: Int J Womens Dermatol Date: 2021-09-09
Authors: Julia Schneider; Lukas Sottmann; Andreas Greinacher; Maximilian Hagen; Hans-Udo Kasper; Cornelius Kuhnen; Stefanie Schlepper; Sven Schmidt; Ronald Schulz; Thomas Thiele; Christian Thomas; Andreas Schmeling Journal: Int J Legal Med Date: 2021-09-30 Impact factor: 2.686
Authors: Andrea Baggiano; Gianpiero Italiano; Marco Guglielmo; Laura Fusini; Andrea Igoren Guaricci; Riccardo Maragna; Carlo Maria Giacari; Saima Mushtaq; Edoardo Conte; Andrea Daniele Annoni; Alberto Formenti; Maria Elisabetta Mancini; Daniele Andreini; Mark Rabbat; Mauro Pepi; Gianluca Pontone Journal: J Clin Med Date: 2022-01-18 Impact factor: 4.241