Han-Young Jin1, Jonathan R Weir-McCall2, Jonathon A Leipsic3, Jang-Won Son4, Stephanie L Sellers5, Michael Shao6, Philipp Blanke6, Amir Ahmadi7, Martin Hadamitzky8, Yong-Jin Kim9, Edoardo Conte10, Daniele Andreini10, Gianluca Pontone10, Matthew J Budoff11, Ilan Gottlieb12, Byoung Kwon Lee13, Eun Ju Chun14, Filippo Cademartiri15, Erica Maffei16, Hugo Marques17, Pedio de Araujo Goncalves17, Sanghoon Shin18, Jung Hyun Choi19, Renu Virmani20, Habib Samady21, Peter H Stone22, Daniel S Berman23, Jagat Narula24, Leslee J Shaw21, Jeroen J Bax25, Kavitha Chinnaiyan26, Gilbert Raff26, Mouaz H Al-Mallah27, Fay Y Lin28, James K Min28, Ji Min Sung29, Sang-Eun Lee29, Hyuk-Jae Chang29. 1. Department of Radiology, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada; Division of Cardiology, Busan Paik Hospital, Inje University College of Medicine, Busan, South Korea. 2. Royal Papworth Hospital, University of Cambridge School of Clinical Medicine, Cambridge, United Kingdom; Royal Papworth Hospital, Cambridge. 3. Department of Radiology, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada; Centre for Heart Lung Innovation, University of British Columbia and St. Paul's Hospital, Vancouver, British Columbia, Canada. Electronic address: jleipsic@providencehealth.bc.ca. 4. Department of Radiology, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada; Yeungnam University Medical Center, Daegu, South Korea. 5. Department of Radiology, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada; Centre for Heart Lung Innovation, University of British Columbia and St. Paul's Hospital, Vancouver, British Columbia, Canada. 6. Department of Radiology, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada. 7. Centre for Heart Lung Innovation, University of British Columbia and St. Paul's Hospital, Vancouver, British Columbia, Canada. 8. Department of Radiology and Nuclear Medicine, German Heart Center Munich, Munich, Germany. 9. Department of Radiology and Nuclear Medicine, German Heart Center Munich, Munich, Germany; Seoul National University Hospital, Seoul, South Korea. 10. Centro Cardiologico Monzino, IRCCS, Milan, Italy. 11. Department of Medicine, Lundquist Institute at Harbor UCLA Medical Center, Torrance, California. 12. Department of Radiology, Casa de Saude São Jose, Rio de Janeiro, Brazil. 13. Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. 14. Seoul National University Bundang Hospital, Seoul, South Korea. 15. Cardiovascular Imaging Center, SDN Foundation IRCCS, Naples, Italy. 16. Department of Radiology, Area Vasta 1/Azienda Sanitaria Unica Regionale (ASUR) Marche, Urbino, Italy. 17. UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, NOVA Medical School, Lisbon, Portugal. 18. National Health Insurance Service Ilsan Hospital, Goyang, South Korea. 19. Busan National University Hospital, Busan, South Korea. 20. Department of Pathology, CVPath Institute, Gaithersburg, Maryland. 21. Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia. 22. Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. 23. Department of Imaging, Cedars-Sinai Medical Center, Cedars-Sinai Heart Institute, Los Angeles, California. 24. Icahn School of Medicine at Mount Sinai, Mount Sinai Heart, Zena and Michael A. Wiener Cardiovascular Institute, and Marie-Josee and Henry R. Kravis Center for Cardiovascular Health, New York, New York. 25. Department of Cardiology, Heart Lung Center, Leiden University Medical Center, Leiden, the Netherlands. 26. Department of Cardiology, William Beaumont Hospital, Royal Oak, Michigan. 27. King Saud Bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research Center, King Abdulaziz Cardiac Center, Ministry of National Guard, Health Affairs, Riyadh, Saudi Arabia. 28. Dalio Institute of Cardiovascular Imaging, New York-Presbyterian Hospital and Weill Cornell Medical College, New York, New York. 29. Division of Cardiology, Department of Internal Medicine, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea; Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Centre, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea.
Abstract
OBJECTIVES: The aim of the current study was to explore the impact of plaque calcification in terms of absolute calcified plaque volume (CPV) and in the context of its percentage of the total plaque volume at a lesion and patient level on the progression of coronary artery disease. BACKGROUND: Coronary artery calcification is an established marker of risk of future cardiovascular events. Despite this, plaque calcification is also considered a marker of plaque stability, and it increases in response to medical therapy. METHODS: This analysis included 925 patients with 2,568 lesions from the PARADIGM (Progression of Atherosclerotic Plaque Determined by Computed Tomographic Angiography Imaging) registry, in which patients underwent clinically indicated serial coronary computed tomography angiography. Plaque calcification was examined by using CPV and percent CPV (PCPV), calculated as (CPV/plaque volume) × 100 at a per-plaque and per-patient level (summation of all individual plaques). RESULTS: CPV was strongly correlated with plaque volume (r = 0.780; p < 0.001) at baseline and with plaque progression (r = 0.297; p < 0.001); however, this association was reversed after accounting for plaque volume at baseline (r = -0.146; p < 0.001). In contrast, PCPV was an independent predictor of a reduction in plaque volume (r = -0.11; p < 0.001) in univariable and multivariable linear regression analyses. Patient-level analysis showed that high CPV was associated with incident major adverse cardiac events (hazard ratio: 3.01: 95% confidence interval: 1.58 to 5.72), whereas high PCPV was inversely associated with major adverse cardiac events (hazard ratio: 0.529; 95% confidence interval: 0.229 to 0.968) in multivariable analysis. CONCLUSIONS: Calcified plaque is a marker for risk of adverse events and disease progression due to its strong association with the total plaque burden. When considered as a percentage of the total plaque volume, increasing PCPV is a marker of plaque stability and reduced risk at both a lesion and patient level. (Progression of Atherosclerotic Plaque Determined by Computed Tomographic Angiography Imaging [PARADIGM]; NCT02803411).
OBJECTIVES: The aim of the current study was to explore the impact of plaque calcification in terms of absolute calcified plaque volume (CPV) and in the context of its percentage of the total plaque volume at a lesion and patient level on the progression of coronary artery disease. BACKGROUND:Coronary artery calcification is an established marker of risk of future cardiovascular events. Despite this, plaque calcification is also considered a marker of plaque stability, and it increases in response to medical therapy. METHODS: This analysis included 925 patients with 2,568 lesions from the PARADIGM (Progression of Atherosclerotic Plaque Determined by Computed Tomographic Angiography Imaging) registry, in which patients underwent clinically indicated serial coronary computed tomography angiography. Plaque calcification was examined by using CPV and percent CPV (PCPV), calculated as (CPV/plaque volume) × 100 at a per-plaque and per-patient level (summation of all individual plaques). RESULTS: CPV was strongly correlated with plaque volume (r = 0.780; p < 0.001) at baseline and with plaque progression (r = 0.297; p < 0.001); however, this association was reversed after accounting for plaque volume at baseline (r = -0.146; p < 0.001). In contrast, PCPV was an independent predictor of a reduction in plaque volume (r = -0.11; p < 0.001) in univariable and multivariable linear regression analyses. Patient-level analysis showed that high CPV was associated with incident major adverse cardiac events (hazard ratio: 3.01: 95% confidence interval: 1.58 to 5.72), whereas high PCPV was inversely associated with major adverse cardiac events (hazard ratio: 0.529; 95% confidence interval: 0.229 to 0.968) in multivariable analysis. CONCLUSIONS: Calcified plaque is a marker for risk of adverse events and disease progression due to its strong association with the total plaque burden. When considered as a percentage of the total plaque volume, increasing PCPV is a marker of plaque stability and reduced risk at both a lesion and patient level. (Progression of Atherosclerotic Plaque Determined by Computed Tomographic Angiography Imaging [PARADIGM]; NCT02803411).
Authors: Amirala Bakhshian Nik; Hooi Hooi Ng; Manuel Garcia Russo; Francesco Iacoviello; Paul R Shearing; Sergio Bertazzo; Joshua D Hutcheson Journal: J Cardiovasc Dev Dis Date: 2022-05-25
Authors: Ya-Jing Qiu; Jun-Yi Luo; Fan Luo; Xin-Xin Tian; Lu Zeng; Zhuo-Ran Zhang; Xiao-Mei Li; Yi-Ning Yang Journal: Front Cardiovasc Med Date: 2022-07-25