Whether it is spontaneous, as in the case of ACS, or iatrogenic, as in the case of percutaneous transluminal coronary angioplasty, platelet deposition occurs almost instantaneously after arterial injury (14). After endothelial denudation, platelets translocate on the vessel wall by an interaction mediated by their constitutively expressed GP Ib-IX-V complex and von Willebrand Factor (vWf) affixed to the subendothelium (15), and possibly also with newly expressed P-selectin on activated endothelial cells (16). The GP Ib-vWF interaction is particularly important under conditions of increased shear stress (17), such as those occurring in stenotic coronary artery lesions. It has also been proposed that vWF may form a bridge between exposed subendothelial collagen and GP Ib on platelets (18), further facilitating the rolling of platelets. After this initial interaction,
Fig. 1. Electron micrographs of resting and activated platelets. The top photographs are scanning electron micrographs of a resting, disc-shaped circulating platelet (upper left; X20,000), and of two activated platelets, which have adopted a spherical form with the formation of long filopodia (upper right; X 10,000). The lower photographs are (from left to right), a schematic depiction of the cross-sectional view of a resting platelet, showing the subcellular platelet structures (bottom left); the actual electron micrograph of a resting platelet (bottom middle; X21,000); and an electron micrograph of an activated platelet, showing the constriction of the microtubular ring around the centralized granules, with the formation of filopodia (bottom right; X 30,000). Reproduced with permission from: George JN. Hemostasis and Fibrinolyisis. In: Stein JH, et al, eds. Internal Medicine, 5th ed. Mosby, St. Louis, 1998:534-540.
platelets decelerate, become activated, and firmly adhere through integrins, most prominently aIIbb3 (also known as GP Ilb/IIIa) and a2Pj (also known as GP Ia/IIa, one of many collagen receptors) (15,18).
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