The role of glycoprotein IIb/IIIa inhibitors in primary percutaneous coronary intervention for ST elevation myocardial infarctionThe opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.

This editorial refers to ‘Three-year duration of benefit from abciximab in patients receiving stents for acute myocardial infarction in the randomized double-blind ADMIRAL study’† by The Admiral Investigators on page 2520 The administration of glycoprotein IIb/IIIa inhibitors is considered to provide additional benefit to mechanical reperfusion in the treatment of patients with ST elevation myocardial infarction and is included as a class-IIa recommendation in the Guidelines for Percutaneous Coronary Intervention of the European Society of Cardiology.1 Glycoprotein IIb/IIIa inhibitors block the surface receptor, which is a member of the integrin superfamily of membrane-bound adhesion molecules. Binding to the major adhesive proteins, fibrinogen and von Willebrand, occurs due to a conformational change of the glycoprotein IIb/IIIa receptor. This final step in platelet aggregation is blocked by the glycoprotein IIb/IIIa inhibitors. Other effects of the glycoprotein IIb/IIIa receptor are interference with thrombus formation, including induction of platelet disaggregation, and reduced clot retraction. Inhibitors developed and used in routine clinical practice include abciximab, the Fab fragment of the chimeric monoclonal antibody, 7E3, and synthetic intravenous administered competitive integrin blocking agents, such as tirofiban and eptifibatide.