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June 26, 1954


Author Affiliations


From the Diabetic Research Laboratory and Medical Services, Maimonides Hospital, and the Department of Medicine, State University of New York, College of Medicine.

JAMA. 1954;155(9):814-817. doi:10.1001/jama.1954.03690270010004

While the pathogenic mechanism responsible for the development of human arteriosclerosis still remains obscure, certain dominant features stand out as playing a role in the development of this morbid condition. Intramural bleeding with resultant inflammatory changes accompanied by deformity of the arterial coats and encroachment on the lumen appears to be one established feature of arteriosclerosis.1 Alterations in the metabolism of cholesterol with an abnormal accumulation of various components of lipids and lipoproteins appear also to play an important part in the development of this disease.2 The higher content of cholesterol in arteriosclerotic coronary arteries makes it necessary to seriously consider a derangement in cholesterol metabolism as a significant factor in atherogenesis.3 However, whether these abnormal accumulations of lipids represent etiological factors or are a biological accompaniment of arteriosclerotic disease has not been established. Certainly the experimental attempts to induce atherosclerosis in animals by means of increasing

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