Comparison of the Morphology of Atherosclerotic Lesions in the Coronary Arteries of Man with Morphology of Lesions Produced and Regressed in Experimental Primates

  • H. C. Stary


Obstructive atherosclerotic lesions produced in nonhuman primates with diets rich in cholesterol decrease in size when a diet that is low in cholesterol is substituted. Small, early lesions disappear completely. The evidence for lesion regression in non-human primates has been reviewed in several recent publications (1–4). In man atherosclerosis regression is also possible but infrequent, as has been shown by investigators who evaluated the angiograms of persons on whom arteriography has been done repeatedly. Table I summarizes 13 studies (5–17) in which decreases in coronary artery obstructions were angiographically documented in 91 of 578 patients who were recatheterized. Forty-five of these improvements surely were caused by lysis of a thrombotic deposit rather than by shrinkage of an established atherosclerotic plaque. Table I does not include studies of sequential coronary arteriograms in which instances of regression were not reported. Therefore, even a larger proportion of human coronary artery lesions than indicated in Table I probably cannot readily regress. Dissimilarities between the lesions of man and experimental primates might be one cause of the dissimilarity in the frequency of documented regression.


Foam Cell Lipid Inclusion Macrophage Foam Cell Extracellular Lipid Lipid Research Clinic Program 
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  1. 1.
    Wissler, R.W., 1978, Current status of regression studies, in: “Atherosclerosis Reviews,” Paoletti, R., and Gotto, A.M., eds., vol. 3, p. 213, Raven Press, New York.Google Scholar
  2. 2.
    Stary, H.C., 1979, Regression of atherosclerosis in primates, Virchows Arch. (Pathol. Anat.), 383: 117.Google Scholar
  3. 3.
    Malinow, M.R., 1980, Atherosclerosis regression in nonhuman primates, Circ. Res., 46: 311.CrossRefGoogle Scholar
  4. 4.
    Clarkson, T.B., Bond, M.G., Bullock, B.C., and Marzetta, CA., 1981, A study of atherosclerosis regression in macaca mulatta IV. Changes in coronary arteries from animals with atherosclerosis induced for 19 months and then regressed for 24 or 48 months at plasma cholesterol concentrations of 300 or 200 mg/dl, Exp. Mol. Pathol., 34: 345.CrossRefGoogle Scholar
  5. 5.
    Gensini, G.G., and Kelly, A.E., 1972, Incidence and progression of coronary artery disease, Arch. Intern. Med. 129: 814.CrossRefGoogle Scholar
  6. 6.
    Bruschke, A.V.G., Proudfit, W.L., and Sones, F.M., 1973, Progress study of 590 consecutive nonsurgical cases of coronary disease followed 5–9 years, Circulation 47: 1154.CrossRefGoogle Scholar
  7. 7.
    Henderson, R.R., Hansing, C. E., Razavi, M., and Rowe, G.G., 1973, Resolution of an obstructive coronary lesion as demonstrated by selective angiography in a patient with transmural myocardial infarction, Am. J. Cardiol., 31: 785.CrossRefGoogle Scholar
  8. 8.
    Buchwald, H., Amplatz, K., Knight, L., Guzman, I., and Varco, R.L., 1978, Arteriography changes after partial ileal bypass, in: “State of Prevention and Therapy in Human Arteriosclerosis and in Animals Models,” Hauss, W.H., et al., eds., Westdeutscher Verlag, Opladen. (Abh. der Rhein.-Westf. Akademie der Wissenschaften, vol. 63, p. 469.)Google Scholar
  9. 9.
    Starzl, T.E., Putnam, C.W., and Koep, L.J., 1978, Portacaval shunt and hyperlipidemia, Arch. Surg., 113: 71.CrossRefGoogle Scholar
  10. 10.
    Rafflenbeul, W., Smith, L.R., Rogers, W.J., Mantle, J.A., Rackley, CE., and Russel, R.O., 1979, Quantitative coronary arteriography. Coronary anatomy of patients with unstable angina pectoris reexamined 1 year after optimal medical therapy, Am. J. Cardiol., 43: 699.CrossRefGoogle Scholar
  11. 11.
    Roth, D., and Kostuk, W.J., 1980, Noninvasive and invasive demonstration of spontaneous regression of coronary artery disease, Circulation, 62: 888.CrossRefGoogle Scholar
  12. 12.
    Thompson, G., Myant, N., Oakley, C, Steiner, R., and Sapsford, R., 1980, Combined medico-surgical strategy for severe familial hypercholesterolemia, in: “Atherosclerosis V,” Gotto, M., et al., eds., p. 454, Springer-Verlag, Berlin-Heidelberg-New York.CrossRefGoogle Scholar
  13. 13.
    Bruschke, A.V.G., Wijers, T.S., Kolsters, W., and Landmann, J., 1981, The anatomic evolution of coronary artery disease demonstrated by coronary arteriography in 256 nonoperated patients, Circulation, 63: 527.CrossRefGoogle Scholar
  14. 14.
    Cowley, M.J., Hastillo, A., Vetrovec, G.W., and Hess, M.L., 1981, Effects of intracoronary streptokinase in acute myo-myocardial infarction, Am. Heart J., 102: 1149.CrossRefGoogle Scholar
  15. 15.
    Rentrop, P., Blanke, H., Karsch, K.R., Kaiser, H., Kostering, H., and Leitz, D., 1981, Selective intracoronary thrombolysis in acute myocardial infarction and unstable angina pectoris, Circulation, 63: 307.CrossRefGoogle Scholar
  16. 16.
    Schroeder, R., Biamino, G., Leitner, V.E.R., and Linderer, T., 1981, Intravenoese streptokinase-infusion bei akutem myokardinfarkt, Dtsch. Med. Wochenschr., 106: 294.CrossRefGoogle Scholar
  17. 17.
    Brown, B.G., Bolson, E.L., and Dodge, H.T., 1982, Arteriographic assessment of coronary atherosclerosis, Arteriosclerosis, 2: 2.CrossRefGoogle Scholar
  18. 18.
    Eggen, D.A. , Strong, J.P., Newman, W.P., Catsulis, C, Malcom, G.T., and Kokatnur, M.A., 1974, Regression of diet-induced fatty streaks in rhesus monkeys, Lab. Invest., 31: 294.Google Scholar
  19. 19.
    Eggen, D.A., 1974, Cholesterol metabolism in rhesus monkey, squirrel monkey, and baboon, J. Lipid Res., 15: 139.Google Scholar
  20. 20.
    Stary, H.C., 1976, Coronary artery fine structure in rhesus monkeys: The early atherosclerotic lesion and its progression, Primates in Medicine, 9: 359.Google Scholar
  21. 21.
    Stary, H.C., Eggen, D.A., and Strong, J.P., 1977, The mechanism of atherosclerosis regression, in: “Atherosclerosis IV,” Schettler, G., et al., eds., p. 394, Springer-Verlag, Berlin-Heidelberg-New York.CrossRefGoogle Scholar
  22. 22.
    Stary, H.C., and Malinow, M.R., 1982, Ultrastructure of experimental coronary artery atherosclerosis in cynomolgus macaques. A comparison with the lesions of other primates, Atherosclerosis, 43: 151.CrossRefGoogle Scholar
  23. 23.
    Stary, H.C., 1983, Structure and ultrastructure of the coronary artery intima in children and young adults up to age 29, in: “Atherosclerosis VI,” Schettler, F.G., et al., eds., p. 82, Springer-Verlag, Berlin-Heidelberg-New York.CrossRefGoogle Scholar
  24. 24.
    Stary, H.C., 1983, Macrophages in coronary artery and aortic intima and in atherosclerotic lesions of children and young adults up to age 29, in: “Atherosclerosis VI,” Schettler, F.G., et al., eds., p. 462, Springer-Verlag, Berlin-Heidelberg-New York.CrossRefGoogle Scholar
  25. 25.
    World Health Organization, 1958, Report of a study group: classification of atherosclerotic lesions, World Health Org. Techn. Rep. Ser. 143.Google Scholar
  26. 26.
    Woolf, N., 1982, “Pathology of Atherosclerosis,” Butterworth Scientific, London.Google Scholar
  27. 27.
    McGill, H.C. Jr., 1977, Atherosclerosis: Problems in pathogenesis, in: “Atherosclerosis Reviews,” Paoletti, R., and Gotto, A.M., eds., vol. 2, p. 27. Raven Press, New York.Google Scholar
  28. 28.
    Hayflick, L., 1975, Current theories of biological aging, Fed. Proc. 34: 9.Google Scholar
  29. 29.
    The Lipid Research Clinics Program Epidemiology Committee, 1979, Plasma lipid distributions in selected North American populations: the lipid research clinics program prevalence study, Circulation, 60: 427.CrossRefGoogle Scholar
  30. 30.
    Rokitansky, C. von, 1852, “Handbuch der Pathologischen Anatomie,” English translation by G.E. Day, vol. 4, p. 261, Sydenham Society, London.Google Scholar
  31. 31.
    Rokitansky, C. von, 1844, “Handbuch der Pathologischen Anatomie,” vol. 2, Braunmuller &Seidel, Vienna.Google Scholar
  32. 32.
    Duguid, J.B., 1946, Thrombosis as a factor in the pathogenesis of coronary atherosclerosis, J. Pathol. Bacteriol., 58: 207.CrossRefGoogle Scholar
  33. 33.
    Duguid, J.B., 1948, Thrombosis as a factor in the pathogenesis of aortic atherosclerosis, J. Pathol. Bacteriol., 60: 57.CrossRefGoogle Scholar
  34. 34.
    McMillan, G.C., 1965, The onset of plaque formation in atherosclerosis, Acta. Cardiol. Suppl. XI: 43.Google Scholar
  35. 35.
    Chandler, A.B., 1972, Thrombosis in the development of coronary atherosclerosis, in: “Atherosclerosis and Coronary Heart Disease,” Likoff, W., et al., eds., p. 28, Grune and Stratton, New York and London.Google Scholar
  36. 36.
    Haust, M.D., 1978, Atherosclerosis in childhood, in: “Perspectives in Pediatric Pathology,” Rosenberg, H.S., and Bolande, R.P., eds., vol. 4, p. 155, Year Book Medical Publishers, Chicago.Google Scholar
  37. 37.
    Woolf, N., 1978, Thrombosis and atherosclerosis, in: “The Thrombogenic Process in Atherogenesis,” Chandler, A.B., et al., eds., Plenum Press, New York. (Adv. Exp. Med. Biol., vol. 104, p. 145).Google Scholar
  38. 38.
    Chandler, A.B., 1975, Relationship of coronary thrombosis to myocardial infarction, Mod. Concepts Cardiovasc. Dis., 44: 1.Google Scholar
  39. 39.
    Goldstein, J.L., and Brown, M.S., 1983, Familial hypercholesterolemia, in: “The Metabolic Basis of Inherited Disease,” Stanbury, J.B., et al., eds., p. 672, McGraw-Hill, New York.Google Scholar
  40. 40.
    Buja, L.M., Kovanen, P.T., and Bilheimer, D.W., 1979, Cellular pathology of homozygous familial hypercholesterolemia, Am. J. Pathol., 97: 327.Google Scholar

Copyright information

© Springer Science+Business Media New York 1984

Authors and Affiliations

  • H. C. Stary
    • 1
  1. 1.Louisiana State University School of MedicineNew OrleansUSA

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