It is known that in untreated atherosclerosis which generally has a progressive course, luminal narrowing by more than 60 % or more by atheromatous plaques is a slow process often lasting decades, whereas rapid thrombotic phenomena may superimpose on this. The present review focuses on the processes of progression and regression only of the atheromatous narrowing. Results obtained from animal experiments and from intervention trials during the past decade using computerized quantitative angiocardiography are discussed. The probable anatomic substrate underlying angiographic regression is dealt with. Furthermore, detection of new lesions by quantitative angiography as well as factors influencing new lesion formation were reviewed. Angiographic trials showed that regression of lesions occurred only in studies in which serum cholesterol levels were reduced, accompanied in some by a rise in HDL-cholesterol. The hypothesis that progression of atherosclerosis is best correIated with LDL-cholesterol, while regression is best related to a rise in HDL-cholesterol is considered.
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