Abstract
Several mechanisms have been suggested by which alterations in plasma lipids may promote thrombosis. Hypercholesterolemia may favor endothelial injury thus triggering early events in thrombogenesis. On the other hand, platelets from patients with familial hypercholesterolemia have high in vitro sensitivity to aggregating agents, increased secretion of nucleotides, and increased formation of thromboxane (1). Evidence is now accumulating that platelet aggregation involves the exposure of receptors for fibrinogen on the platelet surface, and that ADP as well as PG endoperoxides and thromboxane secreted from platelets may play a major role in the exposure of such receptors (2). In this paper we examine the roles of ADP secretion and PG endoperoxide/thromboxane formation in the aggregation and exposure of fibrinogen receptors on platelets from 9 FH patients.
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© 1987 Plenum Press, New York
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Di Minno, G., Cerbone, A.M., Iride, C., Mattioli, P.L., Postiglione, A., Mancini, M. (1987). Platelet Fibrinogen Binding in Familial Hypercholesterolemia. In: Malmendier, C.L., Alaupovic, P. (eds) Lipoproteins and Atherosclerosis. Advances in Experimental Medicine and Biology, vol 210. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1268-0_34
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DOI: https://doi.org/10.1007/978-1-4684-1268-0_34
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4684-1270-3
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