What is the primary mechanism of action of aspirin as an antiplatelet agent?

Aspirin acetylates and irreversibly inhibits cyclooxygenase-1 (COX-1) in platelets. This prevents the synthesis of thromboxane A2 (TXA2), a potent platelet activator and vasoconstrictor. Because platelets lack nuclei and cannot synthesize new COX-1, this effect lasts the lifetime of the platelet (7–10 days). This is why aspirin is used as a long-term antiplatelet agent for cardiovascular prevention. At higher doses, aspirin also inhibits COX-2 (anti-inflammatory/analgesic effect), but the antiplatelet effect is primarily through irreversible COX-1 inhibition.