A Form of Immunological Atherosclerosis

  • Louis Levy
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1)


During the last two decades, the literature on atherosclerosis has become overwhelming. Not only have there been many original scientific contributions, but the subject has been discussed extensively in review articles and books. The pathology observed in human coronary atherosclerosis appears to be unique but does bear some resemblance to certain phases of both induced and spontaneous atherosclerosis in animals. Factors that appear to contribute to both human and animal vascular derangement embrace a wide diversity of stimuli. Dietary components such as lipids have been, and still are, fashionable as pathogenic agents [1]. There is a strong school of thought that believes the early formation of thrombi is of paramount importance in the human disease [2]. The rheologists believe that the turbulence and flow through vessels of certain sizes contribute profoundly to the pathogenesis of atherosclerosis [3]. Other investigators believe that prospective coronary artery disease patients can be found using personality test interviews [4]. Correlations have been found relating coronary heart disease with hypertension, obesity, cigarette smoking, circulating catecholamines, and heredity [5]. It is obvious from the numerous studies by reputable investigators that the formation of the ultimate vascular change called “atheroma” is probably a common result of a variety of stimuli. Not only do these multiple etiologic factors have a similar pathologic manifestation, but also there must be a receptive vessel in an appropriately receptive individual for the formation of an atheromatous lesion.


Foam Cell Cholesterol Diet Fixed Tissue Serum Sickness Large Coronary Artery 
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  1. 1.
    H.F. Watts, “The mechanism of arterial lipid accumulation in human coronary artery atherosclerosis,” in: W. Likoff and J.F. Moyer, Eds., Coronary Heart Disease. New York, Grune & Stratton, 1963.Google Scholar
  2. 2.
    G. Pickering, “Pathogenesis of myocardial and cerebral infarction: modular arteriosclerosis,” Brit. Med. J., 1: 517, 1964.PubMedCrossRefGoogle Scholar
  3. 3.
    M. Texon, “The role of vascular dynamics in the development of atherosclerosis,” in: M. Sander and C. H. Bourne, Eds., Atherosclerosis and Its Origin. New York, Academic Press, 1963.Google Scholar
  4. 4.
    R. H. Rosenman and M. Friedman, “Behavior patterns, blood lipids, and coronary heart disease,” J. Am. Med. Ass., 184: 934, 1963.CrossRefGoogle Scholar
  5. 5.
    J. W. Gofman, Coronary Heart Disease. Springfield, Illinois, Charles C. Thomas, 1959.Google Scholar
  6. 6.
    J. C. Roberts and R. Strauss, Eds., Comparative Atherosclerosis. New York, Hoeber Medical Div. of Harper & Row, 1965.Google Scholar
  7. 7.
    O. Saphir, D. Stryzak, and L. Ohringer, “Hypersensitivity changes in coronary arteries of rabbits and their relationship to arteriosclerosis,” Lab.Invest., 7: 434, 1958.PubMedGoogle Scholar
  8. 8.
    F. G. Germuth, Jr., “A comparative histologic and immunologic study in rabbits of induced hypersensitivity of the serum sickness type,” J. Exptl. Med., 97: 257, 1953.CrossRefGoogle Scholar
  9. 9.
    W.T. Kniker and C. G. Cochrane, “Pathogenic factors in vascular lesions of experimental serum sickness,” J. Exptl. Med., 122: 83, 1965.CrossRefGoogle Scholar
  10. 10.
    S. L. Wilens, “Enhancement of serum sickness lesions in rabbits with pressor agents,” Arch. Pathol., 80: 590, 1965.PubMedGoogle Scholar
  11. 11.
    O. Saphir, M. Telischi, and L. Ohringer, “Rabbit sulfa drug hypersensitivity and lesions resembling arteriosclerosis,” Arch. Pathol., 73: 414, 1962.PubMedGoogle Scholar
  12. 12.
    D.A. Blickens and N.R. DiLuzio, “Induction of phagocytic inhibition and the generalized Shwartzman phenomena by the administration of plasma from reticuloendothelial hypofunctional mice,” J. Reticuloendothelial Soc., 2: 187, 1965.Google Scholar
  13. 13.
    P.D. Mott and S.M. Wolff, “The association of fever and antibody response in rabbits immunized with human serum albumin,” J. Clin. Invest., 45: 372, 1966.PubMedCrossRefGoogle Scholar
  14. 14.
    W. T. Kniker and C. G. Cochrane, “Localization of circulating Ag—Ab complexes in serum sickness,” Federation Proc., 25: 474, 1966.Google Scholar
  15. 15.
    T. Shimamoto, “The relationship of edematous reaction in arteries to atherosclerosis and thrombosis,” J. Atherosclerosis Res., 3: 87, 1963.CrossRefGoogle Scholar
  16. 16.
    D. Harman, “Inhibiting effect of an antihistaminic drug, chlorpheniramine,” Circulation Res., 11: 277, 1963.CrossRefGoogle Scholar
  17. 17.
    T. Shimamoto, F. Numano, and T. Fujita, “Atherosclerosis-inhibiting effect of an antibradykinin agent, pyridanolcarbamate,” Am. Heart J., 71: 216, 1966.PubMedCrossRefGoogle Scholar
  18. 18.
    M. Friedman, S. Byers, and S. St. George, “Cortisone and experimental atherosclerosis,” Arch. Pathol., 77: 56, 1964.Google Scholar
  19. 19.
    L. Levy and G. Cronheim, “Blood levels and clearing activity of a synthetic heparinoid,” Biochem. Pharmacol., 7: 27, 1961.CrossRefGoogle Scholar
  20. 20.
    L. Levy and F. J. Petracek, “Chemical and pharmacological studies on N-resulfated heparin,” Proc. Soc. Exptl. Biol. Med., 190: 901, 1962.Google Scholar

Copyright information

© Springer Science+Business Media New York 1967

Authors and Affiliations

  • Louis Levy
    • 1
  1. 1.Riker LaboratoriesNorthridgeUSA

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