Impact of Non-obstructive left main disease on the progression of coronary artery disease: A PARADIGM substudy

Jonathan R. Weir-McCall, St. Paul's Hospital
Philipp Blanke, St. Paul's Hospital
Stephanie L. Sellers, St. Paul's Hospital
Amir A. Ahmadi, St. Paul's Hospital
Daniele Andreini, IRCCS Centro Cardiologico Monzino
Matthew J. Budoff, The Lundquist Institute
Filippo Cademartiri, IRCCS Fondazione SDN
Kavitha Chinnaiyan, William Beaumont Hospital
Jung Hyun Choi, Pusan National University
Eun Ju Chun, Seoul National University Bundang Hospital
Edoardo Conte, IRCCS Centro Cardiologico Monzino
Ilan Gottlieb
Martin Hadamitzky, Deutsches Herzzentrum München
Yong Jin Kim, Seoul National University Hospital
Byoung Kwon Lee, Severance Hospital
Sang Eun Lee, Severance Hospital
Erica Maffei
Hugo Marques, Hospital da Luz
Gianluca Pontone, IRCCS Centro Cardiologico Monzino
Gilbert L. Raff, William Beaumont Hospital
Sanghoon Shin, National Health Insurance Service Ilsan Hospital
Ji Min Sung, Severance Hospital
Peter Stone, Brigham and Women's Hospital
Habib Samady, Emory University School of Medicine
Renu Virmani, CVPath Institute, Inc.
Jagat Narula, Icahn School of Medicine at Mount Sinai
Daniel S. Berman, Cedars-Sinai Medical Center
Leslee J. Shaw, Emory University School of Medicine
Jeroen J. Bax, Leiden University Medical Center - LUMC
Fay Y. Lin, New York Presbyterian Hospital
James K. Min, New York Presbyterian Hospital
Hyuk Jae Chang, Severance Hospital
Jonathon A. Leipsic, St. Paul's Hospital


© 2018 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.