Formation of a platelet rich white thrombus due to disruption of coronary vascular endothelium is the crucial event in progression of stable angina to acute coronary syndrome (ACS) and complications of percutaneous coronary interventions (PCI).
Atherosclerotic plaque rupture, vascular injury (e.g., from PCI procedures), or denudation of endothelium exposes the subendothelial matrix of the vessel to circulating platelets. Subsequent activation of platelets results in a conformational change in the Glycoprotein (GP) IIb/IIIa present in the platelet membrane thereby activating it's receptor function for fibrinogen and Von Willebrand factor in the plasma. Fibrinogen and Von Willebrand factor link the GP IIb/IIIa from the adjacent platelets leading to their aggregation and thus thrombus formation. This binding of fibrinogen and Von Willebrand factor to the platelet membrane glycoprotein IIb/ IIIa receptor is the final common pathway by which the activated platelets aggregate to form a platelet rich white thrombus irrespective of initial activating stimulus. Eptifibatide blocks this final common pathway and has been approved as a new drug for ACS by The Drug Controller General of India in August 1999.
