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Angiographic, Morphologic, and Angiochemical Changes

Ralph G. DePalma, MD; LeRoy Klein, MD, PhD; Errol M. Bellon, MD; Simon Koletsky, MD

Arch Surg. 1980;115(11):1268-1278.

Abstract
• On a diet with high levels of cholesterol and sucrose, a β-lipoproteinemia developed in rhesus monkeys that is similar to type II human hyperlipidemia. Lesion regression appeared in response to drastic lowering of serum cholesterol (SC) levels. This experiment analyzed angiochemical responses on the addition of a bile-acid sequestrant to continued atherogenic feeding, which resulted in ranges of moderate cholesterolemia that mimick those that occur in man. After two years of atherogenic diet, fatty fibrous plaques were demonstrated in ten monkeys; then cholestyramine resin, 1.5 g/100 g of the atherosclerotic diet, was added to the food of eight monkeys, whereas two served as controls during a 12-month regression period. Six adult control monkeys that did not receive the atherosclerotic diet were also killed. Seven experimental animals overall showed plaque regression when SC level fell from 400 ± 130 to 237 ± 74 mg/dL; one animal showed angiographic combinations of progression and regression. Angiochemical evaluation demonstrated discordant data with instances of decreased plaque cholesterol content and increased levels of collagen. On the average, plaque regression and final composition were related to absolute levels of SC reduction induced by cholestyramine. Regression required that the threshold levels of cholesterol be below 200 mg/dL. Plaques regressed mainly by lipid absorption; in this experiment and, in particular, arterial segments, collagen content sometimes increased.

(Arch Surg 115:1268-1278, 1980)

Author Affiliations
From the Department of Surgery, School of Medicine, University of Nevada, Reno (Dr DePalma), and the Departments of Orthopedic Surgery (Dr Klein), Radiology (Dr Bellon), and Pathology (Dr Koletsky), Case Western Reserve University School of Medicine, Cleveland. Dr Koletsky died May 16, 1980.

Footnotes
Accepted for publication July 31, 1980.

Read before the 28th scientific meeting of the International Cardiovascular Society, Chicago, June 27, 1980.

Reprint requests to Department of Surgery, University of Nevada School of Medicine, 855 Mill St, Reno, NV 89502 (Dr DePalma).

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