Alterations in the Arterial Wall with Aging

  • Richard W. St. Clair


At this meeting we have been considering a variety of factors that might be altered with aging and consequently play a role in exacerbating the development of atherosclerosis. Much of what has been considered falls into the category of “risk factors” that are present in the blood, such as changes in plasma lipoproteins, blood pressure, hormones, etc. A variety of studies have indicated that the commonly accepted risk factors can account for only a portion of the variability in cardiovascular disease. Estimates range from upwards of 50% when clinical events are considered (1) to less than 20% when extent and severity of atherosclerosis is evaluated at autopsy (2). This suggests that there are either additional, yet-to-be-described risk factors or, just as likely, that there are differences at the level of the arterial wall that influence the susceptibility to development of atherosclerosis when exposed to the same risk factors. Studies with animal models, such as pigeons, suggest these differences could be genetically mediated (3). If one accepts the possibility that differences in susceptibility and resistance to atherosclerosis may, in part, be mediated at the level of the arterial wall, then we must begin to understand the mechanisms responsible for this effect if we ever expect to fully explain individual differences in atherosclerosis. It is likely that such differences will be mediated at the levels of the cellular elements of the arterial wall.


Smooth Muscle Cell Arterial Wall Atherosclerotic Lesion Foam Cell Plasma Lipoprotein 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Goldbourt U, Neufeld HN: Genetic aspects of arteriosclerosis. Arteriosclerosis 1986; 6:357–377.PubMedCrossRefGoogle Scholar
  2. 2.
    Holme I, Enger SC, Helgeland A, Hjermann I, Leren P, Lund-Larsen PG, Solberg LA, Strong JP: Risk factors and raised atherosclerotic lesions in coronary and cerebral arteries. Statistical analysis from the Oslo Study. Arteriosclerosis 1981; 1:250–256.PubMedCrossRefGoogle Scholar
  3. 3.
    St. Clair RW: Metabolic changes in the arterial wall associated with atherosclerosis in the pigeon. Fed Proc 1983; 42:2480–2485.Google Scholar
  4. 4.
    Fowler S, Shio H, Haley NJ: Characterization of lipid-laden aortic cells from cholesterol-fed rabbits. IV. Investigation of macrophage-like properties of aortic cell populations. Lab Invest 1979; 41:372–378.PubMedGoogle Scholar
  5. 5.
    Lewis JC, Taylor RG, White MS: Monocyte (MC) migration and endothelial (EC) turnover: Simultaneous events at the edge of atherosclerotic lesions. Circulation 1983; 68:III-300.Google Scholar
  6. 6.
    Schaffner T, Taylor K, Bartucci EJ, Fischer-Dzoga K, Beeson JH, Glagov S, Wissler RW: Arterial foam cells with distinctive immunomorphologic and histochemical features of macrophages. Am J Pathol 1980; 100:57–80.PubMedGoogle Scholar
  7. 7.
    Gordon S: Biology of the macrophage. J Cell Sci 1986; Suppl 4:267–286.Google Scholar
  8. 8.
    Brown MS, Goldstein JL: Lipoprotein metabolism in the macrophage: Implications for cholesterol deposition in atherosclerosis. Ann Rev Biochem 1983; 52:223–261.PubMedCrossRefGoogle Scholar
  9. 9.
    Ghidoni JJ, O’Neal RM: Recent advances in molecular pathology. A review of ultrastructure of human atheroma. Expt Mol Pathol 1967; 7:378–400.CrossRefGoogle Scholar
  10. 10.
    Gown AM, Tsukado T, Ross R: Human atherosclerosis, II. Immunocytochemical analysis of the cellular composition of human atherosclerotic lesions. Am J Pathol 1986; 125:191–207.PubMedGoogle Scholar

Copyright information

© Springler-Verlag New York Inc. 1987

Authors and Affiliations

  • Richard W. St. Clair

There are no affiliations available

Personalised recommendations