Rupture of the atherosclerotic plaque exposes the subendothelial collagen to the bloodstream [Kumar V, et al. Basic Pathology. 5th Edition. Philadelphia, W.B. Saunders Co., 1992]. On contact with collagen, platelets become activated, with platelet adhesion, secretion of platelet contents, and platelet aggregation at the site of injury. The activated platelet surface is an essential catalytic surface for several coagulation reactions that generate thrombin, a key factor in the coagulation sequence [D’Souza D, et al. Lancet. 1994;344:991].
Platelets adhere to exposed subendothelium through interaction with a variety of platelet surface receptors, the most important of which is GP-Ib-IX [Hirsch J, et al. In: Colman RW, et al (eds). Hemostasis and Thrombosis: Basic Principles and Clinical Practice, Third Edition. Philadelphia, J.B. Lipincott Company, 1994:1151]. This glycoprotein is the main receptor for the subendothelial protein ligand von Willebrand factor (vWF).
Platelet aggregation requires the platelet membrane glycoprotein integrin receptor (GP IIb-IIIa), which — at least under low fluid shear stress conditions — is involved in calcium-dependent interplatelet bridging by bound fibrinogen.
Acute Ischemic Stroke: New Concepts of Care
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