Physical Biochemistry of the Lesions of Man, Subhuman Primates, and Rabbits

  • David A. Waugh
  • Donald M. Small
  • Richard W. St. Clair


Our task is to summarize briefly the biochemical constituents of the vessel walls and how these change during the progression from normal intima to an atherosclerotic plaque. The intima is made up of a variety of cellular and noncellular components, including endothelial and occasional smooth muscle cells, glycosaminoglycans, collagen, and elastin ground substances. There is evidence that all of these intimai constituents undergo some changes during the progression from normal intima to atherosclerotic lesion. The major changes in mass and therefore volume during the progression to atherosclerotic lesions in man are in the lipid constituents of the vessel wall. In the normal vessel wall at different ages the total dry weight of the intima contains only a very few percent of its total mass as lipid (1); in the discrete small lesions called fatty streaks the lipid content of the intima in that lesion has increased to approximately 20% of the total mass. However, in carefully dissected, large, raised lesions described as atherosclerotic plaques, the percent dry weight is often greater than 50% (2). Since the density of the lipids is some 30–40% less than the density of the other constituents (proteins, polysaccharides), absolute volume occupied would be greater than the mass. Thus in human atherosclerotic lesions lipids account for a major fraction of the nonwater volume occupied by the lesion and therefore must be considered in the pathogenesis. The rest of this discussion will be directed mainly towards lipids, although other substances which increase in mass during the development of atherosclerotic lesions also include some cellular and connective tissue elements.


Arterial Wall Atherosclerotic Lesion Cholesteryl Ester Foam Cell Free Cholesterol 
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© Springer-Verlag New York Inc. 1983

Authors and Affiliations

  • David A. Waugh
  • Donald M. Small
  • Richard W. St. Clair

There are no affiliations available

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