Aspirin irreversibly blocks cyclooxygenase, an enzyme that in the platelet stimulates arachidonic acid conversion to thromboxane A 2 and in the blood vessel wall promotes prostacyclin synthesis. The net effect of aspirin in ischemic arterial beds depends on the balance between thromboxane A 2, a potent vasoconstrictor and platelet-aggregation agent, and prostacyclin, a vasodilator and platelet-aggregation inhibitor. Since prostacyclin synthesis is stimulated at lower aspirin levels than is thromboxane A2 conversion, treatment plans often use low-dose strategies (e.g., 81 mg/day). For more rapid antiplatelet effect, a medium or higher dose (e.g., 162
Aspirin is quickly absorbed in the upper gastrointestinal tract, reaches peak blood concentrations in 15 to 20 min, and circulates with a half-life of 30 to 60 min. However, its inhibitory effect is irreversible and lasts for the life span of the platelet (about 10 days). The bleeding time (BT) has been sometimes used to detect the antiplatelet activity of aspirin, but virtually all recognize that BT has poor reproducibility, sensitivity, and specificity when used to measure platelet-aggregation abnormalities.
Side effects are mainly gastrointestinal and dose related, and may be reduced with concomitant use of antacids, enteric coating, and buffering agents. Aspirin should be avoided in patients with known hypersensitivity and used cautiously in those with bleeding disorders or severe hepatic disease. Active gastrointestinal hemorrhage (e.g., bleeding peptic ulcer) is a contraindication to aspirin use. However, in AMI and unstable angina with occult gastrointestinal bleeding (e.g., guaiac-positive stool), most experts favor aspirin use with careful monitoring.14 Aspirin therapy is also associated with a slightly increased risk of hemorrhagic stroke (12 per 10,000 over 3 years), but this risk is more than counterbalanced by a tenfold reduction in the risk of myocardial infarction and a threefold reduction in the risk of ischemic stroke. 15
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