What is the mechanism of action of aspirin?

Aspirin's mechanism of action primarily revolves around its ability to inhibit the production of thromboxane A2. Thromboxane A2, a potent vasoconstrictor and promoter of platelet aggregation, is produced in platelets via the cyclooxygenase (COX) pathway. When aspirin is administered, it acetylates the cyclooxygenase enzyme, leading to a reduction in thromboxane A2 synthesis.

By decreasing the levels of thromboxane A2, aspirin effectively reduces platelet activation and aggregation, which is a key factor in preventing thrombotic events such as myocardial infarctions and strokes. This action is particularly beneficial in patients at high risk for cardiovascular complications, as it alters the hemostatic balance in favor of preventing unwanted clot formation.

While inhibiting factor Xa, blocking platelet aggregation, and activating antithrombin III are important processes in hemostasis and thrombosis management, they do not directly describe the primary mechanism by which aspirin exerts its antiplatelet effects. Aspirin does not act on factor Xa nor directly activate antithrombin III, and while its action leads to reduced platelet aggregation, the specific mechanism is through the inhibition of thromboxane A2 production.