Platelet aggregation inhibitors work in different places of the clotting cascade and prevent platelet adhesion, therefore no clot formation.
Aspirin, the most commonly used antiplatelet drug changes the balance between prostacyclin (which inhibits platelet aggregation) and thromboxane (that promotes aggregation). It irreversibly inhibits the enzyme cyclo-oxygenase, which leads to reduction in thromboxane synthesis in platelets and prostacyclin in vascular endothelial cells. The vascular endothelium recovers and can synthesize more prostacyclin but thromboxane synthesis only recovers after new platelets are formed.
Platelet aggregation inhibitors are used acutely in myocardial infarction, atrial fibrillation, following coronary bypass, angioplasty and stenting. It is also used as prophylaxis to prevent myocardial infarction and stroke.
