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HENRY HAIMOVICI, M.D.; NELICIA MAIER, M.D., Ph.D.

AMA Arch Surg. 1961;82(1):1-7.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Ever since 1913, when Anitschkow¹ had induced in the rabbit atheromatous lesions by cholesterol feeding, a great deal of clinical and experimental evidence has been accumulated showing that atherosclerosis is the result of an abnormal lipid metabolism.² This view is based on extensive investigations of the chemical composition of the blood in atherosclerosis. In contrast to the evergrowing literature dealing with the chemical changes of the circulating blood, there is surprisingly little information concerning the role played by the arterial wall in atherogenesis. This situation led G. Lyman Duff to state that "the casual reader of recent literature might wonder whether some authors conceive of an atherosclerosis so independent of the substrate of the vessel wall, that it may occur in the absence of the blood vessels themselves."³

Experimental atherosclerosis in the dog and rabbit carried out by us since 1954 with special reference to the susceptibility . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

From the Vascular Service, Surgical Division, and the Henry and Lucy Moses Surgical Research Laboratories, Montefiore Hospital.

Footnotes
Submitted for publication June 16. 1960.

Supported by U.S. Public Health Service Grant H-3444.

Presidential Address presented at the Eighth Scientific Meeting of the International Cardiovascular Society, North American Chapter, Miami Beach, June 11, 1960.

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