title: Routine early eptifibatide versus delayed provisional use at percutaneous coronary intervention in high-risk non-ST-segment elevation acute coronary syndromes patients: an analysis from the Early Glycoprotein IIb/IIIa Inhibition in Non-ST-Segment Elevation Acute Coronary Syndrome trial.
abstract: OBJECTIVE
  In the EARLY ACS trial, routine early eptifibatide was not superior to delayed provisional use at percutaneous coronary intervention (PCI); however, among PCI-treated patients, numerically fewer ischemic end points occurred in the upstream eptifibatide group. We sought to further explore this finding using methods for examination of treatment effect in this postrandomization subgroup.
  
  
  RESULTS
  Of 9,406 patients in the EARLY ACS primary analysis cohort, 9,166 (97.4%) underwent coronary angiography. We used Cox proportional hazards regression modeling, with PCI as a time-dependent covariate, to examine the effect of routine early versus delayed provisional eptifibatide among 5,541 patients undergoing PCI and to explore the interaction between treatment with PCI and randomized treatment strategy. After multivariable adjustment, compared with delayed provisional use, routine early eptifibatide was associated with lower rate of 30-day death or myocardial infarction (MI) after PCI (hazard ratio [HR] 0.80, 95% CI 0.68-0.95) but not with medical management (HR 0.97, 95% CI 0.74-1.29); PCI × randomized treatment interaction term P = .24. Excluding PCI-related MI, the adjusted HR for 30-day death or MI for routine early eptifibatide versus delayed provisional use was 0.80 (95% CI 0.60-1.08) for post-PCI treatment and 1.01 (95% CI 0.79-1.34) for medical management; PCI × randomized treatment interaction term P = .28.
  
  
  CONCLUSIONS
  Consistent with previous literature, upstream treatment with eptifibatide was associated with improved outcomes in high-risk non-ST-segment elevation acute coronary syndrome patients treated with PCI; however, a nonsignificant interaction term precludes a definite conclusion.
authors.affiliation: Duke Clinical Research Institute, Duke University Medical Center, Durham, NC.
authors.forename: Akshay
authors.initials: A
authors.lastname: Bagai
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: White
authors.forename: Yuliya
authors.initials: Y
authors.lastname: Lokhnygina
authors.forename: Robert P
authors.initials: RP
authors.lastname: Giugliano
authors.forename: Frans
authors.initials: F
authors.lastname: Van de Werf
authors.forename: Gilles
authors.initials: G
authors.lastname: Montalescot
authors.forename: Paul W
authors.initials: PW
authors.lastname: Armstrong
authors.forename: Pierluigi
authors.initials: P
authors.lastname: Tricoci
authors.forename: C Michael
authors.initials: CM
authors.lastname: Gibson
authors.forename: Robert M
authors.initials: RM
authors.lastname: Califf
authors.forename: Robert A
authors.initials: RA
authors.lastname: Harrington
authors.forename: L Kristin
authors.initials: LK
authors.lastname: Newby
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy / Q000401:mortality / Q000628:therapy*; D000368:Aged; D000077542:Eptifibatide; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000209:etiology*; D010455:Peptides / Q000008:administration & dosage*; D062645:Percutaneous Coronary Intervention; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000008:administration & dosage*; D016016:Proportional Hazards Models; D012306:Risk; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077542:Eptifibatide