Friday, June 9, 2023
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Leon H. Charney Professor of Cardiovascular Medicine; Director, Marc and Ruti Bell Vascular Biology Program; Director, Center for the Prevention of Cardiovascular Disease, New York University School of Medicine, New York, New York
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Looking back at animal and clinical studies published since the 1920s, the notion of rapid regression and stabilization of atherosclerosis in humans has evolved from a fanciful goal to one that might be achievable pharmacologically, even for advanced plaques. Our review of this literature indicates that successful regression of atherosclerosis generally requires robust measures to improve plasma lipoprotein profiles. Examples of such measures include extensive lowering of plasma concentrations of atherogenic apolipoprotein B (apoB)-lipoproteins and enhancement of ‘reverse’ lipid transport from atheromata into the liver, either alone or in combination. Possible mechanisms responsible for lesion shrinkage include decreased retention of apoB-lipoproteins within the arterial wall, efflux of cholesterol and other toxic lipids from plaques, emigration of foam cells out of the arterial wall, and influx of healthy phagocytes that remove necrotic debris and other components of the plaque. Unfortunately, the clinical agents currently available cause less dramatic changes in plasma lipoprotein levels, and, thereby, fail to stop most cardiovascular events. Hence, there is a clear need for testing of new agents expected to facilitate atherosclerosis regression. Additional mechanistic insights will allow further progress.
The idea that human atheromata can regress at all has met considerable resistance over the decades.[1,2] Resistance to the idea of lesion regression is strengthened by the fact that advanced atheromata in humans and in animal models contain components that give an impression of permanence, such as necrosis, calcification and fibrosis. In addition, numerous theories have been proposed to explain atherogenesis that include processes thought to be difficult, if not impossible, to reverse including oxidation,[3] injury,[4] and cellular transformations resembling carcinogenesis.[5]
In this Review we summarize the failure of many established and experimental interventions to induce plaque regression, and examine other data indicating that sufficiently drastic changes in the plaque environment can stabilize and cause regression of even advanced lesions.
