Abstract
In the event the circulating platelets come into contact with bare collagen in the subendothelial layer of the vascular wall due to a rupture of a atherosclerotic plaque, their adhesion takes place in this location. The balance of pro-aggregation and anti-aggregation activities is decisive whether the adhesion changes into a platelet thrombus.
The currently used drugs may, however, block the platelet activation in various levels. Inhibitors of the glycoprotein receptors type IIb/IIIa act in the final step of the pathways leading to the platelet activation and in consequence they block the platelet aggregation as a response to all of the agonists.
Currently, they have the most effective the anti-platelet drugs. It has been proved that their administration to patients with an acute coronary syndrome improves both the short-term prognosis as well as the long-term survival.