Glycoprotein IIb/IIIa inhibitors in clinical practice.

Glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitors were developed in the early 1990’s with the purpose of providing maximum platelet aggregation blockade. At first they were used adjunctly with balloon coronary angioplasty to reduce acute occlusion of the vessel treated and its complications such as periprocedural acute myocardial infarction (MI). The dissection of the vessel after balloon dilation in percutaneous coronary intervention (PCIs) occurred in 20 to 25% of the cases, and, as a consequence, acute occlusion developed in 5% of these patients1. Reduction in platelet aggregation with GP IIb/IIIa inhibitors caused a reduction in major cardiovascular events (death, MI and urgent target vessel revascularization/TVR) after PCI2. However, it was the advent of coronary stents, because they reestablish the vessel geometry and “seal” the dissections, which contributed the most to eliminate such complications. GP IIb/IIIa inhibitors, as adjuncts to coronary stents, basically reduced periprocedural MI which occurs due to slow flow phenomena subsequent to platelet embolization (“slow reflow”, “no reflow”) or secondary branch occlusion. The good results of initial studies such as EPIC2, EPILOG3 and EPISTENT4 with the combined reduction of major cardiovascular events (MACEs) determined a growing use of GP IIb/IIIa inhibitors. Since then, different drugs of this class (abciximab, tirofiban and eptifibatide) have been tested in different situations such as elective procedures; acute coronary syndromes (ACSs) with or without ST segment elevation; reduction of coronary restenosis and more recently as a complementary medication to facilitate primary angioplasty.