title: Optimal platelet inhibition in patients undergoing PCI: data from the Multicenter Registry of High-Risk Percutaneous Coronary Intervention and Adequate Platelet Inhibition (MR PCI) study.
abstract: BACKGROUND
  Optimal inhibition of platelet aggregation (IPA) may afford greater protection against ischemic events during percutaneous coronary intervention (PCI). The objective of this study was to test several antiplatelet regimens in elective high-risk PCI patients by comparing different combinations of glycoprotein IIb/IIIa inhibitors and clopidogrel.
  
  
  METHODS
  The study was a randomized open-label study at 3 heart centers in India. One hundred twenty patients were enrolled between July 2006 and September 2006. Patients were randomized to 1 of the 4 groups: group A--tirofiban, group B--eptifibatide, group C--tirofiban + clopidogrel 600-mg loading dose, and group D--eptifibatide + clopidogrel 600-mg loading dose. All patients received a clopidogrel maintenance dose after PCI. The primary outcome measure was the IPA assessed at 10 minutes, at 6 to 8 hours, and at 24 hours.
  
  
  RESULTS
  The IPA was higher with high-dose tirofiban compared with eptifibatide at 10 minutes (95.88 +/- 5.85% vs 91.22 +/- 7.52%, P = .003) and at 6 to 8 hours (93.11 +/- 7.6% vs 85.45 +/- 11.03, P < .001). Significantly more patients achieved >95% IPA with the high-dose tirofiban regimen.
  
  
  CONCLUSIONS
  This head-to-head study comparing high-dose tirofiban with double-bolus eptifibatide demonstrated higher degree of platelet inhibition with high-dose tirofiban at 10 minutes and at 6 to 8 hours in patients undergoing elective high-risk PCI. The addition of clopidogrel did not acutely extend the IPA from intravenous glycoprotein IIb/IIIa inhibitors, but did so at 24 hours.
authors.affiliation: Spandan Heart Institute, Nagpur, India.
authors.forename: H M
authors.initials: HM
authors.lastname: Mardikar
authors.forename: M S
authors.initials: MS
authors.lastname: Hiremath
authors.forename: David J
authors.initials: DJ
authors.lastname: Moliterno
authors.forename: Rony
authors.initials: R
authors.lastname: Mathew
authors.forename: Rangolee
authors.initials: R
authors.lastname: Arora
authors.forename: Dhananjay
authors.initials: D
authors.lastname: Deo
authors.forename: J S
authors.initials: JS
authors.lastname: Hiremath
authors.forename: N V
authors.initials: NV
authors.lastname: Deshpande
authors.forename: Aziz
authors.initials: A
authors.lastname: Khan
authors.forename: Jacob
authors.initials: J
authors.lastname: Joseph
authors.forename: Debabrata
authors.initials: D
authors.lastname: Mukherjee
mesh_terms: D000789:Angina, Unstable / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary; D000077144:Clopidogrel; D000077542:Eptifibatide; D006801:Humans; D009203:Myocardial Infarction / Q000628:therapy*; D010455:Peptides / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D012042:Registries; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000077466:Tirofiban; D014443:Tyrosine / Q000031:analogs & derivatives / Q000627:therapeutic use
chemical_list: D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014443:Tyrosine; D000077144:Clopidogrel; D000077466:Tirofiban; D000077542:Eptifibatide; D013988:Ticlopidine