Omar Dzaye1, Alexander C Razavi1, Michael J Blaha1, Martin Bødtker Mortensen1,2. 1. Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins Hospital, Baltimore, Maryland, USA. 2. Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Abstract
PURPOSE OF REVIEW: To provide a summary of recent literature on the relative impact of luminal stenosis versus atherosclerotic plaque burden in atherosclerotic cardiovascular disease (ASCVD) risk stratification and management. RECENT FINDINGS: Recent results from both randomized controlled clinical trials as well as observational cohort studies have demonstrated that ASCVD risk is mediated mainly by the extent of atherosclerotic disease burden rather than by the presence of coronary stenosis or inducible ischemia. Although patients with obstructive CAD are generally at higher risk for ASCVD events than patients with nonobstructive CAD, this is driven by a higher plaque burden in those with obstructive CAD. Accordingly, the ASCVD risk for a given plaque burden is similar in patients with and without obstructive CAD. Accompanying these observations are randomized controlled trial data, which show that optimization of medical therapy instead of early revascularization is most important for improving prognosis in patients with stable obstructive CAD. SUMMARY: Emerging evidence shows that atherosclerotic plaque burden, and not stenosis per se, is the main driver of ASCVD risk in patients with CAD. This information challenges the current paradigm of selecting patients for intensive secondary prevention measures based primarily on the presence of obstructive CAD.
PURPOSE OF REVIEW: To provide a summary of recent literature on the relative impact of luminal stenosis versus atherosclerotic plaque burden in atherosclerotic cardiovascular disease (ASCVD) risk stratification and management. RECENT FINDINGS: Recent results from both randomized controlled clinical trials as well as observational cohort studies have demonstrated that ASCVD risk is mediated mainly by the extent of atherosclerotic disease burden rather than by the presence of coronary stenosis or inducible ischemia. Although patients with obstructive CAD are generally at higher risk for ASCVD events than patients with nonobstructive CAD, this is driven by a higher plaque burden in those with obstructive CAD. Accordingly, the ASCVD risk for a given plaque burden is similar in patients with and without obstructive CAD. Accompanying these observations are randomized controlled trial data, which show that optimization of medical therapy instead of early revascularization is most important for improving prognosis in patients with stable obstructive CAD. SUMMARY: Emerging evidence shows that atherosclerotic plaque burden, and not stenosis per se, is the main driver of ASCVD risk in patients with CAD. This information challenges the current paradigm of selecting patients for intensive secondary prevention measures based primarily on the presence of obstructive CAD.
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