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

Aspirin's mechanism of action as an antiplatelet agent centers on its ability to irreversibly inhibit cyclooxygenase (COX) enzymes. COX is crucial in the conversion of arachidonic acid to thromboxane A2, a potent promoter of platelet activation and aggregation. By inhibiting COX, aspirin reduces the production of thromboxane A2, leading to diminished platelet aggregation.

This effect of aspirin is particularly beneficial in preventing thrombotic cardiovascular events, such as myocardial infarction and stroke, as it prevents the formation of clots that can obstruct blood flow. The irreversible nature of this inhibition means that the effects can last for the lifespan of the platelet (approximately 7-10 days), which is why aspirin is often used in low doses for long-term prevention of cardiovascular events.

The other choices represent different mechanisms that are not related to aspirin’s antiplatelet action. For instance, inhibition of the Na+/K+/2Cl- co-transporter is involved in diuretics, the inhibition of serotonin reuptake pertains to selective serotonin reuptake inhibitors (SSRIs), and blockade of beta-adrenergic receptors relates to medications used for hypertension or heart failure. None of these options contribute