title: Predicting the risk of bleeding during dual antiplatelet therapy after acute coronary syndromes.
abstract: Dual antiplatelet therapy (DAPT) with aspirin + a P2Y12 inhibitor is recommended for at least 12 months for patients with acute coronary syndrome (ACS), with shorter durations considered for patients with increased bleeding risk. However, there are no decision support tools available to predict an individual patient's bleeding risk during DAPT treatment in the post-ACS setting.
  
  
  
  To develop a longitudinal bleeding risk prediction model, we analy sed 9240 patients with unstable angina/non-ST segment elevation myocardial infarction (NSTEMI) from the Targeted Platelet Inhibition to Clarify the Optimal Strategy to Medically Manage Acute Coronary Syndromes (TRILOGY ACS) trial, who were managed without revasculari sation and treated with DAPT for a median of 14.8 months.
  
  
  
  We identified 10 significant baseline predictors of non-coronary artery bypass grafting (CABG)-related Global Use of Strategies to Open Occluded Arteries (GUSTO) severe/life-threatening/moderate bleeding: age, sex, weight, NSTEMI (vs unstable angina), angiography performed before randomi sation, prior peptic ulcer disease, creatinine, systolic blood pressure, haemoglobin and treatment with beta-blocker. The five significant baseline predictors of Thrombolysis In Myocardial Infarction (TIMI) major or minor bleeding included age, sex, angiography performed before randomi sation, creatinine and haemoglobin. The models showed good predictive accuracy with Therneau'sC-indices: 0.78 (SE = 0.024) for the GUSTO model and 0.67 (SE = 0.023) for the TIMI model. Internal validation with bootstrapping gave similarC-indices of 0.77 and 0.65, respectively. External validation demonstrated an attenuatedC-index for the GUSTO model (0.69) but not the TIMI model (0.68).
  
  
  
  Longitudinal bleeding risks during treatment with DAPT in patients with ACS can be reliably predicted using selected baseline characteristics. The TRILOGY ACS bleeding models can inform risk -benefit considerations regarding the duration of DAPT following ACS.
  
  
  
  ClinicalTrials.gov identifier: https://clinicaltrials.gov/ct2/show/NCT00699998.
authors.affiliation: Duke Clinical Research Institute, Durham, USA.|Department of Cardiology and Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
authors.forename: Joakim
authors.initials: J
authors.lastname: Alfredsson
authors.affiliation: Duke Clinical Research Institute, Durham, USA.
authors.forename: Benjamin
authors.initials: B
authors.lastname: Neely
authors.affiliation: Duke Clinical Research Institute, Durham, USA.
authors.forename: Megan L
authors.initials: ML
authors.lastname: Neely
authors.affiliation: Brigham and Women's Hospital Heart & Vascular Center and Harvard Medical School, Boston, USA.
authors.forename: Deepak L
authors.initials: DL
authors.lastname: Bhatt
authors.affiliation: Division of Cardiology, Department of Medicine, St. Michael's Hospital, Toronto, Canada.|Canadian VIGOUR Centre and Division of Cardiology, University of Alberta, Edmonton, Canada.
authors.forename: Shaun G
authors.initials: SG
authors.lastname: Goodman
authors.affiliation: Duke Clinical Research Institute, Durham, USA.|Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, USA.
authors.forename: Pierluigi
authors.initials: P
authors.lastname: Tricoci
authors.affiliation: Department of Medicine, Stanford University, Stanford, USA.
authors.forename: Kenneth W
authors.initials: KW
authors.lastname: Mahaffey
authors.affiliation: Medisch Centrum Alkmaar, Alkmaar, The Netherlands.
authors.forename: Jan H
authors.initials: JH
authors.lastname: Cornel
authors.affiliation: Green Lane Cardiovascular Service, Auckland City Hospital, Auckland, New Zealand.
authors.forename: Harvey D
authors.initials: HD
authors.lastname: White
authors.affiliation: Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
authors.forename: Keith Aa
authors.initials: KA
authors.lastname: Fox
authors.affiliation: Centre for Chronic Disease Control and Public Health Foundation of India, New Delhi, India.
authors.forename: Dorairaj
authors.initials: D
authors.lastname: Prabhakaran
authors.affiliation: Eli Lilly and Company, Indianapolis, USA.
authors.forename: Kenneth J
authors.initials: KJ
authors.lastname: Winters
authors.affiliation: Canadian VIGOUR Centre and Division of Cardiology, University of Alberta, Edmonton, Canada.
authors.forename: Paul W
authors.initials: PW
authors.lastname: Armstrong
authors.affiliation: Duke Clinical Research Institute, Durham, USA.|Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, USA.
authors.forename: E Magnus
authors.initials: EM
authors.lastname: Ohman
authors.affiliation: Duke Clinical Research Institute, Durham, USA.|Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, USA.
authors.forename: Matthew T
authors.initials: MT
authors.lastname: Roe
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy / Q000601:surgery*; D000368:Aged; D000369:Aged, 80 and over; D000077144:Clopidogrel; D001026:Coronary Artery Bypass / Q000379:methods*; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D005500:Follow-Up Studies; D014943:Global Health; D006470:Hemorrhage / Q000139:chemically induced / Q000453:epidemiology*; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000009:adverse effects*; D000068799:Prasugrel Hydrochloride / Q000008:administration & dosage / Q000009:adverse effects*; D018570:Risk Assessment / Q000379:methods*; D013988:Ticlopidine / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives*; D013997:Time Factors
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D013988:Ticlopidine
keywords: hemorrhage; platelets; risk factors