الفهرس 
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Abstract
Platelets participate in the development of coronary heart disease, contributing to atherogenesis as well as coronary thrombosis. The importance of platelets is illustrated by the benefit of antiplatelet therapy with drugs such as aspirin, clopidogrel, and the glycoprotein (GP) IIb/IIIa inhibitors in the treatment of acute and chronic coronary ischemic syndromes and in maintaining long-term patency of intracoronary stents.
In addition to these well recognized antiplatelet agents, many cardiovascular drugs aimed at nonplatelet mechanisms of ischemia may impair platelet function. There is continued interest in the possibility that the antiplatelet effects of cardiac drugs might influence treatment outcomes.
In primary hemostasis, the platelet response to vascular damage leads to the formation of a hemostatic plug at the site of insult. Platelet then interact with elements of the coagulation cascade to facilitate the incorporation of fibrin into the clot, resulting in clot stabilization. This fibrin-rich clot serves as scaffolding for vascular wall remodeling with the fibrinolytic system ultimately restoring vessel patency. Formation of a hemostatic platelet plug involves platelet adhesion, activation, and aggregation.
Both superficial and deep intimal injury disrupt the intact endothelium which normally prevents the adherence of platelets by the production of the antiplatelet agents nitric oxide and prostacyclin. Disruption of the endothelium also exposes collagen; Platelet adhesion is mediated by the binding of platelet receptors to a number of arterial wall receptors, including subendothelial collagen (whose corresponding platelet receptor is glycoprotein Ia/IIa), von Willebrand factor (GP Ib/IX and IIb/IIIa), fibrinogen (IIb/IIIa), and fibronectin.
Following adhesion, multiple metabolic pathways are stimulated, causing a rise in intracellular calcium through release from intracellular stores and influx from the extracellular space, This increase in cytosolic calcium activates phospholipase A2, leading to the formation of thromboxane A2 (TxA2), resulting in platelet shape change and degranulation of storage granules the production of TXA2 and the release of other vasoactive substances from storage granules (including adenosine diphosphate and serotonin) leads to the recruitment of adjacent platelets to the growing platelet plug.