title: Intracoronary use of GP IIb/IIIa inhibitors in percutaneous coronary interventions.
abstract: The glycoprotein (GP) IIb/IIIa receptor is critical to the process of platelet aggregation and thrombus formation as it serves as the final common pathway for platelet aggregation. For this reason, the development of GP IIb/IIIa inhibitors that block fibrinogen binding to the receptor has become an attractive strategy for antiplatelet therapy with an expected strong and specific effect. Presently, there are three commercially available GP IIb/IIIa inhibitors: abciximab, eptifibatide and tirofiban. All three drugs are commonly administered intravenously, and large-scale clinical trials have demonstrated a clear clinical benefit and good safety profile in patients at high risk, especially those undergoing percutaneous coronary interventions (PCI). Recently, several studies tested the intracoronary (IC) route for GP IIb/IIIa inhibitors in order to verify its safety and its possible superiority as compared to the intravenous (IV) route. The majority of the studies testing the IC route were conducted using abciximab and in patients with STEMI with better results in terms of myocardial reperfusion and infarct size and also promising results in terms of clinical outcome. On the IC administration of eptifibatide and tirofiban only some, even if promising, data are available. Larger and randomized studies are warranted to confirm the superiority of the IC route of administration of the GP IIb/IIIa inhibitors to the IV one in patients with coronary artery disease undergoing PCI.
authors.affiliation: Interventional Cardiology, Morgagni-Pierantoni Hospital, Forli, Italy.
authors.forename: Maria
authors.initials: M
authors.lastname: De Vita
authors.forename: Valentina
authors.initials: V
authors.lastname: Coluccia
authors.forename: Francesco
authors.initials: F
authors.lastname: Burzotta
authors.forename: Enrico
authors.initials: E
authors.lastname: Romagnoli
authors.forename: Carlo
authors.initials: C
authors.lastname: Trani
mesh_terms: D000077284:Abciximab; D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000503:physiopathology / Q000601:surgery*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000503:physiopathology / Q000601:surgery; D006328:Cardiac Catheterization; D003131:Combined Modality Therapy; D006333:Heart Failure / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D007263:Infusions, Parenteral; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage* / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077284:Abciximab