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Platelets and Aspirin

Blood clots are formed through the process of hemostasis. In primary hemostasis, platelets activate and aggregate to form a platelet plug. This platelet plug is then strengthened by fibrin and a thrombus is formed during the process of secondary hemostasis. Hemostasis is essential to prevent excessive loss of blood. However, when a thrombus forms inside an artery, it blocks the flow of blood to that tissue. This causes a myocardial infarction, if a coronary artery supplying blood to the muscle of the heart is blocked, or a stroke, if a thrombus forms in an artery supplying blood to the brain. In high-risk patients, it is critical to prevent the formation of thrombi in these arteries. This is where aspirin becomes helpful.
Aspirin prevents thrombi formation by blocking platelet production of thromboxane A2, an essential platelet aggregation component. Aspirin has the ability to suppress the creation of prostaglandins and thromboxane A2 by irreversibly inactivating the cyclooxygenase-1 (COX-1) enzyme. COX-1 plays an important role in prostaglandin and thromboxane A2 synthesis. Although other nonsteroidal anti-inflammatory drugs (NSAIDs) can also inhibit the COX-1 enzyme in a reversible manner, aspirin inhibits the COX-1 enzyme for a greater period of time, thus making it the preferred NSAID for the prevention of ischemic events.