[Pathophysiology of platelet activation and pharmacology of GPIIb/IIIa inhibitors]

PLATELET FUNCTION AND GPIIB/IIA ANTAGONISTS: Inhibition of platelet function can be obtained via two different mechanisms: Interaction with cellular signaling inside the platelet after stimulation by appropriate agonists, such as thrombin, thromboxane A2 or ADP. Alternatively, compounds might interfere directly with the final step, i.e. fibrinogen binding and platelet aggregate formation. This is the mechanism of action of GPIIb/IIIa antagonists, such as abciximab, tirofiban and eptifibatide. These receptor antagonists are platelet-selective because the receptor is only on platelets. Numerous clinical trials have established the usefulness of all three compounds in acute endothelial injury, as associated with percutaneous coronary interventions.

It is currently unknown whether clinically relevant differences exist between the low-molecular weight (tirofiban, eptifibatide) compounds and the antibody abciximab because no direct comparison has been performed yet. However, the TARGET trial (tirofiban vs. abciximab in patients with acute coronary syndromes) is underway and probably will answer this question.