![]() ![]() Simultaneously, collagen also binds von Willebrand factor (vWF) to activate platelets via glycoprotein (GP) Ia/IIa and GP IV receptors. Underlying collagen interacts with tissue factor (TF) to trigger the clotting cascade, activating thrombin, which contributes to platelet adhesion at the injury site. ![]() Under physiological conditions, platelets are activated by a series of intracellular signals when vascular endothelium is damaged. ![]() Salicylates are only briefly mentioned here, primarily in comparing various mechanisms of antiplatelet drugs. As such, a separate monograph specifically devoted to salicylate toxicity is available. When compared to individuals not taking antiplatelet medications, patients on an antiplatelet agent have a 1.5 times greater risk of bleeding, and this increases when taking additional antiplatelet agents. Given the relatively narrow pharmacologic actions of antiplatelet drugs, toxicity primarily confines itself to an increased risk of hemorrhage. Despite a variety of pharmacologic actions, all antiplatelet drugs inhibit platelet activation and aggregation, lowering atherothrombotic related events. These agents are used to decrease major adverse events due to acute coronary syndromes, peripheral vascular disease, and stroke. As the prevalence of cardiovascular disease (CVD) escalates worldwide, so does the use of antiplatelet medications in its management. ![]()
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