Jonathan R Weir-McCall1, Philipp Blanke1, Stephanie L Sellers2, Amir A Ahmadi3, Daniele Andreini4, Matthew J Budoff5, Filippo Cademartiri6, Kavitha Chinnaiyan7, Jung Hyun Choi8, Eun Ju Chun9, Edoardo Conte4, Ilan Gottlieb10, Martin Hadamitzky11, Yong Jin Kim12, Byoung Kwon Lee13, Sang-Eun Lee14, Erica Maffei15, Hugo Marques16, Gianluca Pontone4, Gilbert L Raff7, Sanghoon Shin17, Ji Min Sung14, Peter Stone18, Habib Samady19, Renu Virmani20, Jagat Narula21, Daniel S Berman22, Leslee J Shaw19, Jeroen J Bax23, Fay Y Lin24, James K Min24, Hyuk-Jae Chang14, Jonathon A Leipsic25. 1. St. Paul's Hospital & University of British Columbia, Department of Radiology, Vancouver, British Columbia, Canada. 2. St. Paul's Hospital & University of British Columbia, Department of Radiology, Vancouver, British Columbia, Canada; Centre for Heart Lung Innovation, University of British Columbia & St. Paul's Hospital, Vancouver, British Columbia, Canada. 3. Centre for Heart Lung Innovation, University of British Columbia & St. Paul's Hospital, Vancouver, British Columbia, Canada. 4. Centro Cardiologico Monzino, IRCCS, Milan, Italy. 5. Department of Medicine, Los Angeles Biomedical Research Institute, Torrance, CA, USA. 6. Cardiovascular Imaging Center, IRCCS SDN Foundation, Naples, Italy. 7. Department of Cardiology, William Beaumont Hospital, Royal Oak, MI, USA. 8. Busan University Hospital, Busan, South Korea. 9. Seoul National University Bundang Hospital, 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. Seoul National University College of Medicine, Seoul National University Hospital, South Korea. 13. Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. 14. 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. 15. Department of Radiology, Area Vasta 1/ASUR Marche, Urbino, Italy. 16. UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisbon, Portugal. 17. National Health Insurance Service Ilsan Hospital, South Korea. 18. Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA, USA. 19. Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA. 20. Department of Pathology, CVPath Institute, Gaithersburg, Maryland, USA. 21. 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, NY, USA. 22. Department of Imaging and Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA. 23. Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands. 24. Dalio Institute of Cardiovascular Imaging, New York-Presbyterian Hospital and Weill Cornell Medical College, New York, NY, USA. 25. St. Paul's Hospital & University of British Columbia, Department of Radiology, Vancouver, British Columbia, Canada; Centre for Heart Lung Innovation, University of British Columbia & St. Paul's Hospital, Vancouver, British Columbia, Canada. Electronic address: jleipsic@providencehealth.bc.ca.
Abstract
BACKGROUND: The aim of the study is examine the impact of non-obstructive (<50%stenosis) left main (LM) disease on the natural history of coronary artery disease using serial coronary computed tomography angiography (CTA). METHODS: CTAs from the PARADIGM (Progression of atherosclerotic plaque determined by computed tomographic angiography imaging) study, a prospective multinational registry of patients who underwent serial CTA at a ≥2 year interval were analyzed. Those without evidence of CAD on their baseline scan were excluded, as were those with obstructive left main disease. Coronary artery vessels and their branches underwent quantification of: plaque volume and composition; diameter stenosis; presence of high-risk plaque. RESULTS: Of 944 (62 ± 9 years, 60% male) who had evidence of CAD at baseline, 444 (47%) had LM disease. Those with LM disease had a higher baseline plaque volume (194.8 ± 221mm3 versus 72.9 ± 84.3mm3, p < 0.001) and a higher prevalence of high-risk plaque (17.5% versus 13%, p < 0.001) than those without LM disease. On multivariable general linear model, patients with LM disease had greater annual rates of progression of total (26.5 ± 31.4mm3/yr versus 14.9 ± 20.1mm3/yr, p < 0.001) and calcified plaque volume (17 ± 24mm3/yr versus 7 ± 11mm3/yr, p < 0.001), with no difference in fibrous, fibrofatty or necrotic core plaque components. CONCLUSION: The presence of non-obstructive LM disease is associated with greater rates of plaque progression and a higher prevalence of high-risk plaque throughout the entire coronary artery tree compared to CAD without LM involvement. Our data suggests that non-obstructive LM disease may be a marker for an aggressive phenotype of CAD that may benefit from more intensive treatment strategies.
BACKGROUND: The aim of the study is examine the impact of non-obstructive (<50%stenosis) left main (LM) disease on the natural history of coronary artery disease using serial coronary computed tomography angiography (CTA). METHODS: CTAs from the PARADIGM (Progression of atherosclerotic plaque determined by computed tomographic angiography imaging) study, a prospective multinational registry of patients who underwent serial CTA at a ≥2 year interval were analyzed. Those without evidence of CAD on their baseline scan were excluded, as were those with obstructive left main disease. Coronary artery vessels and their branches underwent quantification of: plaque volume and composition; diameter stenosis; presence of high-risk plaque. RESULTS: Of 944 (62 ± 9 years, 60% male) who had evidence of CAD at baseline, 444 (47%) had LM disease. Those with LM disease had a higher baseline plaque volume (194.8 ± 221mm3 versus 72.9 ± 84.3mm3, p < 0.001) and a higher prevalence of high-risk plaque (17.5% versus 13%, p < 0.001) than those without LM disease. On multivariable general linear model, patients with LM disease had greater annual rates of progression of total (26.5 ± 31.4mm3/yr versus 14.9 ± 20.1mm3/yr, p < 0.001) and calcified plaque volume (17 ± 24mm3/yr versus 7 ± 11mm3/yr, p < 0.001), with no difference in fibrous, fibrofatty or necrotic core plaque components. CONCLUSION: The presence of non-obstructive LM disease is associated with greater rates of plaque progression and a higher prevalence of high-risk plaque throughout the entire coronary artery tree compared to CAD without LM involvement. Our data suggests that non-obstructive LM disease may be a marker for an aggressive phenotype of CAD that may benefit from more intensive treatment strategies.
Authors: Steven J Lahti; David I Feldman; Zeina Dardari; Mohammadhassan Mirbolouk; Olusola A Orimoloye; Albert D Osei; Garth Graham; John Rumberger; Leslee Shaw; Matthew J Budoff; Alan Rozanski; Michael D Miedema; Mouaz H Al-Mallah; Dan Berman; Khurram Nasir; Michael J Blaha Journal: Atherosclerosis Date: 2019-03-24 Impact factor: 5.162