title: [Platelet glycoprotein IIb/IIIa inhibitors in coronary artery disease].
abstract: BACKGROUND
  Inhibition of platelet activity at the injured coronary plaque is a target for novel therapeutic strategies. One of these mechanisms is the blockade of the platelet surface membrane glycoprotein (GP) IIb/IIIa receptor, which binds circulating fibrinogen or von Willebrand factor and crosslinks platelets as the final common pathway to platelet aggregation. Intravenous agents directed against this receptor include the chimeric monoclonal antibody fragment abciximab, the peptide inhibitor eptifibatide and nonpeptide mimetics tirofiban and lamifiban.
  
  
  RESULTS
  During percutaneous coronary intervention, an absolute reduction of 1.5-6.5% in the 30-day risk of death, myocardial infarction or repeat urgent revascularization has been observed, with some variability in treatment effect among the agents tested. Treatment effect is achieved early with every modality of revascularization and maintained over the long-term up to 3 years. Increased bleeding risk may be minimized by reduction and weight adjustment of concomitant heparin dosing. In the acute coronary syndromes without ST segment elevation, absolute 1.5-3.2% reductions in 30-day rates of death or myocardial infarction have been achieved with 2- to 4-day courses of eptifibatide or tirofiban. Clinical benefit accrues during the period of drug infusion and is durable. Treatment effect may be enhanced among patients undergoing early coronary revascularization, with evidence of stabilization before intervention and suppression of postprocedural ischemic events.
  
  
  CONCLUSIONS
  Thus, blockade of the platelet GP IIb/IIIa receptor reduces ischemic complications when used as an adjunct to percutaneous coronary intervention or the management of acute ischemic syndromes.
authors.affiliation: II. Interne Abteilung mit Kardiologie, Allgemeines Offentliches Krankenhaus der Barmherzigen Schwestern vom Heiligen Kreuz, Wels, Austria. johann.auer@khwels.at
authors.forename: Johann
authors.initials: J
authors.lastname: Auer
authors.forename: Robert
authors.initials: R
authors.lastname: Berent
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Lassnig
authors.forename: Thomas
authors.initials: T
authors.lastname: Weber
authors.forename: Edwin
authors.initials: E
authors.lastname: Maurer
authors.forename: Bernd
authors.initials: B
authors.lastname: Eber
mesh_terms: D000077284:Abciximab; D000284:Administration, Oral; D000789:Angina, Unstable / Q000188:drug therapy*; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000627:therapeutic use; D018849:Controlled Clinical Trials as Topic; D001026:Coronary Artery Bypass; D003327:Coronary Disease / Q000188:drug therapy*; D004359:Drug Therapy, Combination; D004562:Electrocardiography; D004630:Emergencies; D000077542:Eptifibatide; D005500:Follow-Up Studies; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000008:administration & dosage / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000188:drug therapy*; D010455:Peptides / Q000008:administration & dosage / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D016032:Randomized Controlled Trials as Topic; D012307:Risk Factors; D015607:Stents; D013577:Syndrome; D013921:Thrombocytopenia / Q000139:chemically induced; D015912:Thrombolytic Therapy; D013997:Time Factors; D000077466:Tirofiban; D014443:Tyrosine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014443:Tyrosine; D000077466:Tirofiban; D000077542:Eptifibatide; D000077284:Abciximab