Histopathology of Arteriosclerosis

  • Michael B. Gravanis

Abstract

Both denuding and nondenuding endothelial injury have been proposed as pathogenetic mechanisms in atherogenesis. Conversion of a nondenuding injury to a denuding one, however, is not considered to be a rare event. Although both mechanisms initiate different molecular pathways, they ultimately lead to 1) proliferation of smooth muscle cells; 2) synthesis of connective tissue matrix; 3) focal accumulation of monocytes/macrophages; 4) lymphocytic infiltration; and 5) variable intracellular and extra-cellular lipid accumulation and eventually stenotic lesions [1].

Keywords

Smooth Muscle Cell Atherosclerotic Plaque Elastic Fiber Lipid Core Original Magnification 
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.

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References

  1. 1.
    Wilcox JN, Harker LA: Molecular and cellular mechanisms of atherogenesis: studies of human lesions linked with animal modeling. In Haemostasis and Thrombosis, edn 3, vol 2. Edited by Bloom AL, Forbes CD, Thomas DP, et al. Edinburgh: Churchill Livingstone; 1993, 1139–1152.Google Scholar
  2. 2.
    Cybulsky MI, Gimbrone MA: Endothelial expression of a mononuclear leukocyte adhesion molecule during atherogenesis. Science 1991, 251: 788–791.PubMedCrossRefGoogle Scholar
  3. 3.
    Celermajer DS: Endothelial dysfunction: does it matter? is it reversible? J AmColl Cardiol 1997, 30: 325–333.CrossRefGoogle Scholar
  4. Bar Shavit R, Benezra M, Sabbah V, et al.: Thrombin as a multifunctional protein: induction of cell adhesion and proliferation. Am J Respir Cell Mol Bio1 1992; 6:123–130.Google Scholar
  5. Shultz PJ, Knauss TC, Mene P, et al.: Mitogenic signals for thrombin in mesangial cells: regulation of phospholipase C and PDGF genes. Am J Physiol 1989, 257(suppl F):366–374.Google Scholar
  6. Zhang Y, Cliff WJ, Schoefl GI, et al.: Plasma protein insudation as an index of early coronary atherogenesis. Am J Pathol 1993, 143:496–505.Google Scholar
  7. Evanko SP, Raines EW, Ross R, et al.: Proteoglycan distribution in lesions of atherosclerosis depends on lesion severity, structural characteristics, and the proximity of platelet-derived growth factor and transforming growth factor-ß. Am J Pathol 1998, 152:533–546.Google Scholar
  8. McEvoy LM, Sun H, Tsao PS, et al.: Novel vascular molecule involved in monocyte adhesion to aortic endothelium in models of atherogenesis. J Exp Med 1997, 185:2069–2077.Google Scholar
  9. 9.
    McGill HC Jr: Persistent problems in the pathogenesis of atherosclerosis. Arteriosclerosis 1984, 4: 443–451.PubMedCrossRefGoogle Scholar
  10. 10.
    Tracy RE, Kissling GE: Age and fibroplasia as preconditions for atheronecrosis in human coronary arteries. Arch Pathol Lab Med 1987, 111: 957–963.PubMedGoogle Scholar
  11. Van Der Wal AC, Das PK, Van Der Berg DB, et al.: Atherosclerotic lesions in humans: in situ immunophenotypic analysis suggesting an immune-mediated response. Lab Invest 1989, 61:166–170.Google Scholar
  12. 12.
    Wilcox JN: Analysis of local gene expression in human atherosclerotic plaques by in situ hybridization. Trends Cardiovasc Med 1991, 1: 17–24.PubMedCrossRefGoogle Scholar
  13. Wilcox JN, Smith KM, Williams LT, et al.: Platelet derived growth factor mRNA detection in human atherosclerotic plaques by in situ hybridization. J Clin Invest 1988, 82:1134–1143.Google Scholar
  14. 14.
    Ross R: The pathogenesis of atherosclerosis: a perspective for the 1990’s. Nature 1993, 362: 801–809.PubMedCrossRefGoogle Scholar
  15. 15.
    Gerrity RG, Goss JA, Soby L: Control of monocyte recruitment by chemotactic factor(s) in lesion-prone areas of swine aorta. Atherosclerosis 1985, 5: 55–66.Google Scholar
  16. 16.
    Rose R: Atherosclerosis: a defence mechanism gone awry. Am J Pathol 1993, 143: 987–1002.Google Scholar
  17. 17.
    Fuster V, Badimon JJ, Badimon L: Clinical-pathological correlations of coronary disease progression and regression. Circulation 1992, 86 (suppl 6): 1–11.Google Scholar
  18. 18.
    Richardson PD, Davies MS, Born GVR: Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques. Lancet 1989, 2: 941–944.PubMedCrossRefGoogle Scholar
  19. Bini A, Fenoglio JJ Jr, Mesa-Tejada R, et al.: Identification and distribution of fibrinogen, fibrin and fibrin(ogen) degradation products in atherosclerosis: use of monoclonal antibodies. Arteriosclerosis 1989, 9:109–121.Google Scholar
  20. Lendon C, Davies M, Born G, et al.: Atherosclerotic plaque caps are locally weakened when macrophage density is increased. Atherosclerosis 1991, 65:302–310.Google Scholar
  21. Amento EP, Ehsani N, Palmer H, et al.: Cytokines positively and negatively regulate interstitial collagen gene expression in human vascular smooth muscle cells. Arterioscler Thromb 1991, 11:1223–1230.Google Scholar
  22. 22.
    Libby P: Molecular bases of the acute coronary syndromes. Circulation 1995, 91: 2844–2850.PubMedCrossRefGoogle Scholar
  23. 23.
    Kovanen PT, Koaartinen M, Paavonen T: Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation 1995, 92: 1084–1088.PubMedCrossRefGoogle Scholar
  24. Nissen S, Gurley J, Booth D, et al.: Differences in ultrasound plaque morphology in stable and unstable patients [abstract]. Circulation 1991, 84:436.Google Scholar
  25. Davies MJ, Richardson PD, Woolf N, et al.: Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophages and smooth muscle cell content. Br Heart J 1993, 69:377–381.Google Scholar
  26. Zhang Y, Cliff WJ, Shoefl GI, et al.: Immunohistochemical study of intimal microvessels in coronary atherosclerosis. Am J Pathol 1993, 43:164–172.Google Scholar
  27. Nicosia RF, Lin YJ, Hazelton D, et al.: Endogenous regulation of angiogenesis in the rat aorta model: role of vascular endothelial growth factor. Am J Pathol 1997, 151:1379–1386.Google Scholar
  28. 28.
    Demer LL: A skeleton in the atherosclerosis closet. Circulation 1995, 92: 2029–2032.PubMedCrossRefGoogle Scholar
  29. Hirota S, Imakita M, Kohri K, et al.: Expression of osteopontin messenger RNA by macrophages in atherosclerotic plaques. Am J Pathol 1993,143:1003–1008.Google Scholar
  30. 30.
    Demer LL: Lipid hypothesis of cardiovascular calcification. Circulation 1997, 95: 297–298.PubMedCrossRefGoogle Scholar
  31. 31.
    Guyton JR, Klemp KF: The lipid-rich core region of human athero- sclerotic fibrous plaques: prevalence of small lipid droplets and vesicles by electron microscopy. Am J Pathol 1989, 134: 705–717.PubMedGoogle Scholar
  32. Podet EJ, Shaffer DR, Gianturco SH, et al.: Interaction of low density lipoproteins with human aortic elastin. Arterioscler Thromb 1991, 1:11:116.Google Scholar
  33. 33.
    Falk E: Why do plaques rupture? Circulation 1992, 86 (suppl III): 30–42.Google Scholar
  34. 34.
    Theroux P, Foster V: Acute coronary syndromes: unstable angina and non-Q-wave myocardial infarction. Circulation 1998, 97: 1195–1206.PubMedCrossRefGoogle Scholar
  35. 35.
    Stary HC: The sequence of cell and matrix changes in atherosclerotic lesions of coronary arteries in the first forty years of life. Eur Heart J 1990, 11 (suppl E): 3–19.PubMedCrossRefGoogle Scholar
  36. 36.
    Davies MJ: Stability and instability: two faces of coronary atherosclerosis. Circulation 1996, 94: 2013–2020.PubMedCrossRefGoogle Scholar
  37. Lewis LC, Bennet-Cain AL, DeMars CS, et al.: Procoagulant activity after exposure of monocyte-derived macrophages to minimally oxidized low density lipoprotein. Am J Pathol 1995, 147:1029–1040.Google Scholar
  38. Shah PK, Falk E, Badimon JJ, et al.: Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques: potential role of matrix-degrading metalloproteinases and implication for plaque rupture. Circulation 1995, 92:1565–1569.Google Scholar
  39. 39.
    Badimon L, Chesebro JH, Badimon JJ: Thrombus formation on ruptured atherosclerotic plaques and rethrombosis on evolving thrombi. Circulation 1992, 86 (suppl 6): 74–85.Google Scholar
  40. 40.
    Nachman RL: Lipoprotein (alpha): molecular mischief in the microvasculature. Circulation 1997, 96: 2485–2487.PubMedGoogle Scholar
  41. Schachinger V, Halle M, Minners J, et al.: Lipoprotein (alpha) selectively impairs receptor-mediated endothelial vasodilator function of the human coronary circulation. J Am Cell Cardiol 1997, 30:927–934.Google Scholar
  42. Lopez-Candales A, Holmes, DR, Liao S, et al.: Decreased vascular smooth muscle cell density in medial degeneration of human abdominal aortic aneurysms. Am J Pathol 1997, 150:993–1007.Google Scholar
  43. Loscalzo J, Weinfeld M, Fless GM, et al.: Lipoprotein (alpha), fibrin binding, and plasminogen activation. Arteriosclerosis 1990, 10:240–245.Google Scholar
  44. Koch AE, Kunkel SL, Pearce WH, et al.: Enhanced production of the chemotactic cytokines interleukin-8, and monocyte chemoattractant protein-1 in human abdominal aortic aneurysms. Am J Pathol 1993, 142:1423–1431.Google Scholar
  45. Hanson GK, Jonasson S, Seifert PS, et al.: Immune mechanisms in atherosclerosis. Arteriosclerosis 1989, 9:567–578.Google Scholar
  46. 46.
    Koch AE, Haines K, Rizzo RJ, et al.: Human abdominal aortic aneurysms: immunophenotypic analysis suggesting an immune-mediated response. Am J Pathol 1990, 137: 1199–1213.PubMedGoogle Scholar

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© Springer Science+Business Media New York 2000

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  • Michael B. Gravanis

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