CV effects of ASA
ASA is a well-established therapy for secondary prevention of myocardial infarction (MI) in patients with known CAD. This is accomplished through inhibition of COX-1 and subsequent decline in TXA 2 , a potent platelet activator. It is an ideal agent for several reasons: (1) COX-1, but not COX-2; is expressed in mature platelets; (2) ASA is a COX-1-specific inhibitor; (3) ASA works through irreversible binding to the COX-1 enzyme, providing stable suppression of enzyme activity; and (4) evidence demonstrates “ASA-triggered” production of antiinflammatory mediators such as lipoxins and resolvins. Other traditional NSAIDs that inhibit COX-1 can reversibly inhibit platelets, but there is no definitive evidence of cardioprotection with these agents.