In the context of coronary artery disease, what is the goal of antiplatelet therapy?

The goal of antiplatelet therapy in the context of coronary artery disease is to prevent plaque rupture. This therapy works by inhibiting platelet aggregation, which plays a crucial role in the formation of blood clots. In coronary artery disease, atherosclerotic plaques can accumulate within the coronary arteries. If these plaques rupture, they can lead to the formation of a thrombus (blood clot) that can obstruct blood flow, resulting in serious events such as myocardial infarction (heart attack).

By using antiplatelet agents, such as aspirin or clopidogrel, the likelihood of thrombus formation after a plaque rupture is significantly reduced. This is particularly important because once a rupture occurs, the risk of severe cardiovascular events increases dramatically.

In contrast, lowering cholesterol levels primarily targets the prevention of plaque formation rather than the prevention of rupture, while decreasing myocardial oxygen demand and managing hypertension address different aspects of heart disease and do not directly affect the stability or integrity of existing plaques. Thus, the primary intention of antiplatelet therapy is to maintain cardiovascular health by preventing the catastrophic events that can arise from plaque instability and rupture.