Details

Autor(en) / Beteiligte

• Malinow, M. Rene[Herausgeber]
• Blaton, Victor H[Herausgeber]

Titel

Regression of Atherosclerotic Lesions : Experimental Studies and Observations in Humans

Ort / Verlag

Boston, MA : Springer US

Erscheinungsjahr

1984

Link zum Volltext

• Volltext

Beschreibungen/Notizen

• I. Regression of Atherosclerosis in Animals -- The Pathobiology of the Atherosclerotic Plaque in the Mid-1980s -- Interaction of Therapeutic Diets and Cholesterol-Lowering Drugs in Regression Studies in Animals -- Progression and Regression of Nonhuman Primate Coronary Artery Atherosclerosis: Considerations of Experimental Design -- The Comparative Pathology of Nonhuman Primate Atherosclerosis -- Plant Glycosides. Effects on Atherosclerosis Regression in Macaca fascicularis -- Plasma Lipoprotein Changes Induced by Diets. Effect on Progression and Regression of Arterial Lesions in Nonhuman Primates -- Regression of Arterial Lesions in Animal Models: Scanning and Transmission Electron Microscopic Aspects -- Use of Cholesteryl Ester Analogs to Study Transport of Lipoproteins in Intact Animals -- Interaction Between Lipids and the Intercellular Matrix of the Arterial Wall: Its Role in the Evolution of the Atherosclerotic Lesion -- II. Studies on Human Atherosclerosis -- The Evolution of
• The Advanced Study Institute on Regression of Atherosclerotic Lesions, sponsored by the North Atlantic Treaty Organization, was held in Maratea, Italy, September 11-13, 1983. The institute was designed to foster discussion of experimental data on the regression of atherosclerosis in animals and evidence of a similar phenomenon in humans. The participating scientists showed with anatomical and biochemical data, that atherosclerosis regresses in cholesterol fed animals after withdrawal of atherogenic stimuli. The existence of regression in humans was inferred from sequential angiographic visualization of arteries, but anatomical and biochemical characteristics of the process have not been defined. Two mechanisms are probably involved in such an angiographic regression. The first, which may occur when hyperlipidemia is partly or fully corrected or during undernutrition or other metabolic abnormalities, may be related to atherosclerosis changes noted in animals undergoing regression. The second type seems independent of changes in plasma lipid levels and may involve resolution of thrombi or other underlying arterial wall factors. The relative frequencies of the two mechanisms are unknown; whether they can occur simultaneously also warrants consideration. It is likely that an exciting milestone will be forthcoming when regression of atherosclerosis is unequivocally demonstrated in humans. Publication of these institute proceedings constitutes a valuable background for future developments