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Drug that inhibits platelet aggregation.
Aspirin inhibition of the enzyme cyclooxygenase-1 (COX-1) in platelets prevents arachidonic acid-induced production of thromboxane A2, a potent mediator of platelet aggregation, as well as vasoconstriction. The half-life of aspirin is only 20 min in the plasma, but due to its irreversible effects on COX-1, the therapeutic effects can last the lifetime of the platelet, up to 1 week following administration (Patrono et al. 1985). Aspirin has been shown to reduce cardiovascular events in the setting of acute myocardial infarction and acute stroke (Antithrombotic Trialists’ (ATT) Collaboration 2002). It is also recommended that aspirin be administered (300–350 mg) to patients undergoing stent placement (Schwartz et al. 1988). Higher doses of aspirin (≥300 mg/day) have been shown to produce a greater effect on COX-2, thereby achieving anti-inflammatory and analgesic properties as well. Aspirin at those higher doses, though, has been shown to have gastrointestinal side effects such as bleeding by eroding the protective prostaglandins in the gut mucosa (Roderick et al. 1993).
For primary prevention of cardiovascular events, meta-analyses have indicated a reduction in myocardial infarction risk that is offset by an increase in risk of major gastrointestinal and extracranial bleeding. However, no reduction in cardiovascular events has been shown in a meta-analysis of studies involving patients with diabetes (Antithrombotic Trialists’ (ATT) Collaboration 2009; Stavrakis et al. 2011).
References and Further Reading
- King, S. B., 3rd, Smith, S. C., Jr., Hirshfeld, J. W., Jr., Jacobs, A. K., Morrison, D. A., Williams, D. O., et al. (2008). 2007 focused update of the ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. Journal of the American College of Cardiology, 51, 172–209.CrossRefGoogle Scholar