Glycoprotein IIb-IIIa inhibitors – Do we still need them?

Platelets play central role in thrombotic events in acute coronary syndromes (ACS) and during percutaneous coronary interventions (PCI). Platelet activation occurs through various mechanisms and all culminate in expression of the surface GP IIb-IIIa receptors which mediate their aggregation and thrombosis. Glycoprotein IIb-IIIa inhibitors (GPI) remain the most powerful antiplatelet agents by inhibiting this final common pathway of platelet activation. The role of GPI in the treatment of coronary ischemic events has evolved through the past 20 years. Given their potent antiplatelet activity and consistent anti-ischemic benefit in major trials, they were an integral part of antiplatelet – antithrombin portfolio in the treatment of ACS and during PCI over a decade. However, the advent of stents and thienopyridine ticlopidine and later clopidogrel made periprocedural ischemic complications less common and GPI had slowly lost its importance in routine low-risk PCI. Though GPI reduced periprocedural ischemic complications, increased bleeding events continued to be a major problem. In the recent years, bleeding has increasingly been recognized as a major determinant of clinical outcomes both with ACS and PCI. Recently, the availability of bivalirudin as an equally effective and safer periprocedural anticoagulant, heparin and GPI have slowly been pushed to second place over the entire spectrum of coronary interventions. The newer antiplatelets which provide rapid and more consistent antiplatelet action further reduced the role of GPI to a very small subset of patients where ischemic risk far exceeds the thrombotic risk.1–3 This editorial briefly evaluates the current role of GPI in the background of recent major studies with newer antiplatelets and bivalirudin.