What is the mechanism of action of aspirin in cardiovascular therapy?

Aspirin’s primary mechanism of action in cardiovascular therapy involves the inhibition of platelet aggregation through the inhibition of cyclooxygenase (COX) enzymes. Aspirin irreversibly acetylates the COX-1 enzyme in platelets, leading to a decrease in the formation of thromboxane A2, a potent aggregator of platelets and vasoconstrictor. By reducing thromboxane A2 production, aspirin effectively diminishes the ability of platelets to aggregate, thereby reducing the risk of thrombus formation in various cardiovascular conditions, particularly in the context of preventing myocardial infarction and stroke.

This mechanism is crucial for managing patients with cardiovascular diseases as it helps maintain blood flow and minimizes the risk of clot formation that can obstruct arteries. The other options do not pertain to the role of aspirin in this context; for instance, activating protein kinases or decreasing renin levels relates to different pathways that are not directly linked to platelet function or cardiovascular events, while inhibiting viral DNA polymerase pertains to antiviral medications and is irrelevant to aspirin’s action.