The Current Role of Glycoprotein IIb/IIIa Inhibitors in Percutaneous Coronary Intervention

Abstract

The central role of platelets in acute coronary syndromes (ACS) and percutaneous coronary interventions (PCI) is well appreciated. The various platelet activation mechanisms finally lead to expression and activation of surface glycoprotein IIb/IIIa receptors that mediate platelet aggregation and thrombus formation. Glycoprotein IIb/IIIa inhibitors (GPIs) are the most potent antiplatelent agents and their role in ACS treatment and PCI has been dominant in the recent past. The advent of stents and thienopyridines minimized ischemic complications and in parallel the role of GPIs in low risk PCI. Despite being effective in decreasing PCI-related ischemic complications, the major drawback of GPI use is a relative increase of bleeding that can adversely affect prognosis. The availability of bivalirudin, which is regarded as an equally effective but safer antithrombotic agent when compared to the combination of heparin and GPIs, despite an ongoing controversy, has also led to a decrease of GPI use in PCI for ACS. Finally the advent of novel potent antiplatelet agents (prasugrel, ticagrelor and soon cangrelor) further contained GPI use in patients with ischemic – thrombotic risk that clearly exceeds bleeding risk and mainly for bail-out in case of a thrombotic event during PCI. A concise overview of accumulated data regarding optimal use of GPIs as determined by large clinical trials and recent guidelines is herein attempted.