Hypercholesterolemia and Platelets

  • Robert S. Lees
  • Angelina C. A. Carvalho
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 104)


Many lines of evidence have linked the circulating plasma lipoproteins with thrombosis, and both with atherosclerosis. Many theories of atherogenesis include mural thrombosis as one of the inciting factors, or the sole inciting factor, for atherosclerotic plaque formation. Clinically, elevated plasma lipids and increased concentrations of circulating lipoproteins have been known for years to predispose to early and severe atherosclerosis and its thrombotic complications. Familial hypercholesterolemia (Type II hyperlipoproteinemia) in particular, especially in the homozygous state, is associated with a very high incidence of premature, severe, and often generalized atherosclerosis (1). Over the past 7 years, we have studied the relationships among hyperlipoproteinemia, platelet function, soluble coagulation parameters, and clinical evidence of atherosclerosis and thrombosis. Our results suggest that patients with Type II hyperlipoproteinemia have a particular predisposition to thrombosis because of increased platelet function, both in comparison with normal subjects, and with patients with other forms of hyperlipoproteinemia. Laboratory studies suggest that these differences may be mediated through alterations in platelet fatty acid metabolism in hypercholesterolemia, particularly in thromboxane formation from arachidonate. In this paper, we shall review our data on platelet function in hyperlipoproteinemia.


Arachidonic Acid Free Cholesterol Thrombotic Complication Familial Hypercholesterolemia Phosphatidyl Inositol 
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.
    Lees, R.S., Wilson, D.E., Schonfeld, G., and Fleet, S. (1973) Prog. Med. Genetics 9, 237–290.Google Scholar
  2. 2.
    Hatch, F.T., and Lees, R.S. (1968) Adv. in Lipid Res. 6, 1–68.Google Scholar
  3. 3.
    Lees, R.S., and Hatch, F.T. (1963) J. Lab. Clin. Med. 61, 518–528.PubMedGoogle Scholar
  4. 4.
    Fredrickson, D.S., and Lees, R.S. (1965) Circulation 31, 321–327.PubMedCrossRefGoogle Scholar
  5. 5.
    Carvalho, A.C., Lees, R.S., Vaillancourt, R.A., and Colman, R.W. (1977) Circulation 56, 114–118.PubMedCrossRefGoogle Scholar
  6. 6.
    Carvalho, A.C., Colman, R.W., and Lees, R.S. (1974) N. Engl. J. Med. 290, 434–438.PubMedCrossRefGoogle Scholar
  7. 7.
    Born, G.V.R. (1962) Nature (Lond.) 194, 927–929.CrossRefGoogle Scholar
  8. 8.
    Carvalho, A.C., Colman, R.W., and Lees, R.S. (1974) Circulation 50, 570–574.PubMedCrossRefGoogle Scholar
  9. 9.
    Wolfe, S.M., and SHulman, N.R. (1970) Biochem. Biophys. Res. Comm. 41, 128–234.PubMedCrossRefGoogle Scholar
  10. 10.
    Bartlett, G.R. (1959) J. Biol. Chem. 234, 466–468.PubMedGoogle Scholar
  11. 11.
    Skipski, V.P., Peterson, R.F., and Barclay, M. (1964) Biochem. J. 90, 374–378.Google Scholar
  12. 12.
    Bizios, R., Wong, L.K., Vaillancourt, R., Lees, R.S., and Carvalho, A.C. (1977) Thrombosis and Haemostasis 38, 228.Google Scholar
  13. 13.
    Steele, P., and Rainwater, J. (1977) Circulation 56 (III), 120.Google Scholar
  14. 14.
    Carvalho, A.C., Lees, R.S., Vaillancourt, R.A., Cabral, R.B., Weinberg, R.M., and Colman, R.W. (1976) Thromb. Res. 8, 843857.Google Scholar
  15. 15.
    Hamberg, M., Svenson, J., and Samuelsson, B. (1975) Proc. Nat. Acad. Sci. USA 72, 2994–2998.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1978

Authors and Affiliations

  • Robert S. Lees
    • 1
  • Angelina C. A. Carvalho
    • 1
  1. 1.Arteriosclerosis CenterMassachusetts Institute of TechnologyCambridgeUSA

Personalised recommendations