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(Circulation. 1999;99:e1-e11.)
© 1999 American Heart Association, Inc.

Circulation Electronic Pages

Evaluation of Platelet Membrane Glycoproteins in Coronary Artery Disease

Consequences for Diagnosis and Therapy

Meinrad Gawaz, MD; Franz-Josef Neumann, MD; Albert Schömig, MD

From 1 Medizinische Klinik, Klinikum rechts der Isar und Deutsches Herzzentrum, Technische Universität München, München, Germany.

Correspondence to Meinrad Gawaz, MD, 1 Medizinische Klinik, Klinikum rechts der Isar und Deutsches Herzzentrum, Technische Universität München, Lazarettstraße 36, 80636 München, Germany. E-mail gawaz@dhm.mhn.de

Key Words: platelets • glycoproteins • coronary disease • thrombosis • platelet aggregation inhibitors

Platelets and Arterial Thrombosis

Platelets play a fundamental role in atherogenesis and development of ischemic complications.^{1 2 3} Under physiological conditions, platelets do not interact with the vessel wall. Injury of vascular intima disrupts the antithrombotic properties of endothelium and exposes the blood to adhesive molecules of the subendothelium. Platelet adhesion to the damaged vessel wall is the first step in hemostasis and thrombosis.⁴ Platelet adhesion is followed by spreading and activation, resulting in release of granule components and aggregate formation.^{5 6} On initial contact, platelet glycoprotein (GP) Ib/V/IX complex binds to von Willebrand factor associated with collagen on the subendothelial surface (Figure 1)^{4 5} and thus arrests the platelet on the vessel surface. The collagen receptor ₂ß₁ is an important secondary receptor for platelet adhesion. ₂ß₁-Collagen interaction leads to platelet activation and is critical for the spreading process involving the fibrinogen receptor GP IIb/IIIa to ensure close contact of the spread platelet with the surface.⁵ Other adhesion receptors, including the fibronectin receptor ₅ß₁ and the laminin receptor ₆ß₁, support and strengthen secondary adhesion (Figure 1). The fibrinogen receptor GP IIb/IIIa is particularly important in platelet-platelet coadhesion, termed aggregation. This requires conformational changes in GP IIb/IIIa that allow binding of soluble fibrinogen to the platelet membrane (Figure 2). Thus, fibrinogen bridging allows formation of platelet aggregates (Figure 2).^{6 7 8 9}

View larger version (37K): [in this window] [in a new window]   Figure 1. Platelet membrane glycoproteins and primary hemostasis. vWF indicates von Willebrand factor; Fn, fibronectin; Col, collagen; Lam, laminin; and AA, arachidonic acid.

View larger version (23K): [in this window] [in a new window]   Figure 2. Platelet aggregation. Epi indicates epinephrine; Col, collagen; and Fg, . . . [Full Text of this Article]

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