What is the mechanism of action of aspirin in acute coronary syndrome?

• A. Irreversibly inhibits COX-1, reducing thromboxane A2 and platelet aggregation.
• B. Reversibly inhibits COX-2, reducing inflammation only.
• C. Increases platelet aggregation.
• D. Blocks beta-adrenergic receptors.

Answer: (A)

Aspirin in acute coronary syndrome works by irreversibly inhibiting COX-1 in platelets, which stops the production of thromboxane A2, a potent promoter of platelet aggregation and vasoconstriction. Because platelets lack nuclei, they cannot synthesize new COX-1, so this inhibition lasts for the life of the platelet (about 7 to 10 days). This sustained reduction in thromboxane A2 prevents further platelet clumping at sites of plaque rupture, helping to limit thrombus growth and improve outcomes in ACS.

At higher doses, aspirin can also affect COX-2 and inflammation, but the critical antithrombotic effect in ACS comes from the irreversible COX-1 inhibition in platelets. The other options describe mechanisms that don’t match aspirin’s action: reversible COX-2 inhibition would mainly reduce inflammation, increasing platelet aggregation would worsen thrombosis, and blocking beta-adrenergic receptors is unrelated to platelet function.