What mechanism allows aspirin to help prevent clot formation in coronary arteries?

Aspirin is effective in preventing clot formation in coronary arteries primarily because it inhibits platelet aggregation. When a blood vessel is injured, platelets are activated and clump together to form a clot, which can lead to obstruction of blood flow. Aspirin works by irreversibly inhibiting an enzyme called cyclooxygenase-1 (COX-1), which is crucial for the production of thromboxane A2. Thromboxane A2 is a substance that promotes platelet activation and aggregation. By inhibiting this pathway, aspirin effectively reduces the ability of platelets to clump together, thereby lowering the likelihood of clot formation in the arteries.

Other mechanisms mentioned, such as reducing inflammation or promoting vasodilation, do not directly contribute to the prevention of clot formation in the context of acute coronary events. While they may be beneficial in other contexts, they are not the primary action of aspirin in the prevention of coronary artery clots. Additionally, increasing blood viscosity would have an opposite effect by potentially increasing the risk of clot formation rather than preventing it.