title: Chronic vitamin K antagonist therapy and bleeding risk in ST elevation myocardial infarction patients.
abstract: OBJECTIVE
  Acute management of ST elevation myocardial infarction (STEMI) patients on chronic vitamin K antagonist (VKA) therapy is uncertain. This study aims to estimate in-hospital major bleeding risk among STEMI patients on chronic VKA treated with primary percutaneous coronary intervention (PCI); and determine the relationship between bleeding and acute treatments stratified by international normalised ratio (INR) values.
  
  
  METHODS
  We retrospectively examined 120,270 STEMI patients treated with primary PCI at 586 national registry hospitals (2007-2012).
  
  
  RESULTS
  Overall, 3101 patients (2.6%) were on VKA which was associated with increased in-hospital major bleeding risk when compared with patients not on VKA (17.0%, vs 10.1%; adjusted OR 1.26, 95% CI 1.13 to 1.40). In patients on VKA, admission INR ≥2.0 was not associated with an increase in bleeding risk compared to INR <2.0. Patients on VKA were more likely to receive clopidogrel or bivalirudin within 24 h of presentation (acute), but less likely to receive prasugrel, heparin, or glycoprotein IIb/IIIa inhibitors (GPI). In those patients, acute GPI was associated with increased bleeding risk (adjusted OR 1.92, 95% CI 1.54 to 2.40) while bivalirudin was associated with decreased risk (adjusted OR 0.69, 95% CI 0.55 to 0.86); bleeding risk associated with heparin, bivalirudin, ADP-receptor blockers, or GPI was similar between INR ≥2.0 and <2.0.
  
  
  CONCLUSIONS
  In STEMI patients treated with primary PCI, chronic VKA therapy was associated with a significant increase in in-hospital major bleeding risk compared to no VKA therapy, irrespective of whether admission INR was ≥2.0 or not. In patients on VKA, GPI was associated with increased bleeding risk while bivalirudin was associated with decreased risk.
authors.affiliation: UnityPoint Clinic-St Luke's Hospital, Cedar Rapids, Iowa, USA.
authors.forename: Wassef
authors.initials: W
authors.lastname: Karrowni
authors.affiliation: Duke Clinical Research Institution, Duke University Medical Center, Durham, North Carolina, USA.
authors.forename: Tracy Y
authors.initials: TY
authors.lastname: Wang
authors.affiliation: Duke Clinical Research Institution, Duke University Medical Center, Durham, North Carolina, USA.
authors.forename: Anita Y
authors.initials: AY
authors.lastname: Chen
authors.affiliation: Duke Clinical Research Institution, Duke University Medical Center, Durham, North Carolina, USA.
authors.forename: Laine
authors.initials: L
authors.lastname: Thomas
authors.affiliation: NorthShore University HealthSystem, Evanston, Illinois, USA.
authors.forename: Jorge F
authors.initials: JF
authors.lastname: Saucedo
authors.affiliation: University of Iowa Carver College of Medicine, Iowa City, Iowa, USA.
authors.forename: Ramzi N
authors.initials: RN
authors.lastname: El Accaoui
mesh_terms: D000368:Aged; D000925:Anticoagulants / Q000009:adverse effects*; D016009:Chi-Square Distribution; D005260:Female; D006470:Hemorrhage / Q000097:blood / Q000139:chemically induced*; D006760:Hospitalization; D006801:Humans; D019934:International Normalized Ratio; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis / Q000628:therapy*; D016017:Odds Ratio; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects; D012042:Registries; D012189:Retrospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D016896:Treatment Outcome; D014481:United States; D014812:Vitamin K / Q000037:antagonists & inhibitors*
chemical_list: D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D014812:Vitamin K