Left main coronary atherosclerosis progression, constrictive remodeling, and clinical events

Abstract

<h4>Objectives</h4>The aim of this study was to evaluate the progression of atherosclerosis within the left main coronary artery (LMCA) in association with risk factor modifying therapies.<h4>Background</h4>Despite studies demonstrating slowing of disease progression within epicardial coronaries with risk factor modification, little is known about the natural history and clinical sequelae of atherosclerosis progression within the LMCA.<h4>Methods</h4>In 340 patients with angiographic coronary artery disease who underwent serial intravascular ultrasound imaging to evaluate the effects of anti atherosclerotic therapies across 7 clinical trials, LMCA and epicardial disease progression was characterized. Relationships between changes in plaque burden with remodeling parameters and the incidence of major adverse cardiovascular events (MACE) (death, myocardial infarction, hospital stay for unstable angina, and coronary revascularization) were investigated.<h4>Results</h4>Plaque regression was observed in the LMCA segment, and progression was observed in adjacent epicardial segments (percent atheroma volume [PAV] -0.39 ± 0.1% vs. +0.37 ± 0.1%, p < 0.001). Changes in LMCA lumen volume correlated strongly with changes in external elastic membrane (beta coefficient 0.91, p < 0.001) and negatively with the change in PAV (beta coefficient -0.55, p < 0.001). Patients who experienced a MACE had smaller baseline LMCA minimum lumen area (11.6 vs. 12.2 mm(2), p = 0.05) and greater progression of PAV in the LMCA (+0.51 ± 0.3% vs. -0.35 ± 0.2%, p = 0.02) compared with those who were MACE-free. Significant reductions from baseline in both external elastic membrane (-4.7 ± 1.7 mm(3), p < 0.01) and lumen volumes (-4.0 ± 1 mm(3), p < 0.01) were also observed in those having an event.<h4>Conclusions</h4>Left main coronary atherosclerosis responds to systemic risk factor modification. Patients experiencing a MACE were more likely to demonstrate progressive disease and constrictive arterial remodeling within the LMCA segment.