Hypercholesterolemia and Platelets
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.
KeywordsArachidonic Acid Free Cholesterol Thrombotic Complication Familial Hypercholesterolemia Phosphatidyl Inositol
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