The PTCA procedure, due to rupturing the clot and damaging the endothelium at the site of the clotted coronary artery, causes an exploded activation of the coagulation cascade and accents the critical role of the platelets in mediating ischemic complications resulting from the PTCA.

Inhibiting GPIIb/IIIa receptors is an extremely potent form of anti-platelet therapy that can result in a dramatic reduction in the risk of death and myocardial infarction. The introduction of the murine/human chimeric antibody fragment c7E3Fab (abciximab, ReoPro) has resulted in the widespread availability and increasing clinical use of this therapy. Several synthetic forms of GPIIb/IIIa antagonists were recently approved, such as Aggrastat (tirofiban) and Integrilin (eptifibatide).

However, too much platelet inhibition or too slow a platelet recovery may shift the prothrombotic state into hemorrhage.

Coronary Artery Bypass Graft (CABG)
Liver transplantation
Exposure to artificial surface devices (ASD)
Percutaneous Coronary Angioplasty (PTCA)
Disseminated Intravascular Coagulation (DIC)