How does Aspirin function as an antiplatelet agent?

Aspirin functions as an antiplatelet agent primarily by inhibiting the cyclooxygenase (COX) enzyme, which is crucial in the synthesis of thromboxane A2 (TXA2). Thromboxane A2 is a potent promoter of platelet aggregation and vasoconstriction. When aspirin irreversibly inhibits COX-1, it reduces the production of TXA2 in platelets. This reduction leads to decreased platelet activation and aggregation, effectively lowering the risk of thrombus formation, which is critical in preventing cardiovascular events such as heart attacks and strokes.

Moreover, the irreversible nature of aspirin's effect on COX means that the inhibition lasts for the lifespan of the affected platelets, which is about 7 to 10 days. Consequently, this characteristic makes aspirin a long-lasting antiplatelet agent, providing sustained benefits in reducing the risk of arterial thrombus formation without requiring frequent dosing.

In contrast, the other options do not accurately describe aspirin's mechanism of action. For example, increasing thromboxane A2 production or enhancing platelet aggregation would lead to increased thrombus risk, which is opposite to what aspirin aims to achieve. Blocking P2Y12 receptors is a mechanism associated with other antiplatelet