title: The complementary use of glycoprotein IIb/IIIa inhibitors and drug-eluting stents in contemporary percutaneous coronary intervention.
abstract: The percutaneous treatment of symptomatic, obstructive coronary artery disease continues to undergo evolutionary changes that have led to an increase in the number of procedures performed each year. Studies on the adjunctive use of thienopyridines and glycoprotein (GP) IIb/IIIa inhibitors during and following percutaneous coronary intervention (PCI) have demonstrated a reduction in the ischemic complications following PCI. One of the GP IIb/IIIa inhibitors, abciximab, has been shown to reduce mortality one year after successful PCI compared with placebo. Despite the reduction in ischemic complications and a potential reduction in mortality at one year, the antiplatelet agents have not consistently been shown to affect the rates of restenosis following PCI. Recent, exciting data on the use of drug-eluting stents (DES) in diseased coronary vessels has generated immense enthusiasm within the interventional community about the future ability to dramatically reduce the rates of restenosis following PCI with the use of this novel stent technology. With the introduction and assumed widespread use of these new stents, it appears that the contemporary interventional cardiologist will now have two complementary therapies available for use during percutaneous revascularization: GP IIb/IIIa inhibitors for the reduction of ischemic complications during and immediately following PCI, and DES for the prevention of long-term restenosis within the treated vessel segment. Caution should be taken not to view these valuable therapies as mutually exclusive but rather to recognize that each addresses critical aspects of percutaneous revascularization that have been improved upon after being studied in thousands of patients in controlled, randomized clinical trials.
authors.affiliation: Division of Cardiology, Duke Clinical Research Institute, Duke University Medical Center, Durham, NC, 27710, USA.
authors.forename: Charles E
authors.initials: CE
authors.lastname: Mayes
authors.forename: David E
authors.initials: DE
authors.lastname: Kandzari
authors.forename: Pascal J
authors.initials: PJ
authors.lastname: Goldschmidt-Clermont
authors.forename: Harry R
authors.initials: HR
authors.lastname: Phillips
mesh_terms: D000077284:Abciximab; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D000077542:Eptifibatide; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use*; D017202:Myocardial Ischemia / Q000503:physiopathology / Q000628:therapy*; D010455:Peptides / Q000627:therapeutic use*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D017410:Practice Guidelines as Topic; D015607:Stents; D000077466:Tirofiban; D014443:Tyrosine / 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