title: Impact on Patient Management and Outcome of Switching between 2 Contemporary Sensitive Cardiac Troponin Assays.
abstract: BACKGROUND
  Myocardial infarction is characterized by an increase of cardiac troponin I (cTnI) above the 99th percentile of a reference population. Our hospital switched from 1 contemporary cTnI assay to another and observed a doubling of cTnI results above the assays' respective 99th percentile cutoffs. We investigated the potential impact on inpatient management and outcomes.
  
  
  METHODS
  We performed a retrospective cohort study of 45 498 individuals with ≥1 cTnI result between January 2013 and June 2014. The Dimension cTnI assay was used in 2013; the Abbott Architect cTnI assay was used in 2014.
  
  
  RESULTS
  Before switching cTnI assays, 19.2% (4742/30 872) of patients had at least 1 of the first 3 cTnIs above the 99th percentile (0.07 μg/L). After switching to the Architect cTnI assay, 31.4% (4034/14 626) of patients had at least 1 cTnI above the 99th percentile (0.03 μg/L). This increase was due to the difference in the assays' 99th percentile cutoffs. Having an increased cTnI reported on the Architect assay that would not have been reported as such on the Dimension assay (0.03-0.06 μg/L) correlated with increased inpatient mortality, length of stay, non-ST elevation myocardial infarction diagnosis, therapeutic heparin use, and percutaneous coronary intervention, relative to individuals with cTnI <0.03 μg/L.
  
  
  CONCLUSIONS
  The changes observed in patient outcomes and management were likely due to the increased sensitivity and lower 99th percentile cutoff of the Architect assay. It is important to recognize the potential impact that differences in sensitivity and assay configuration may have on patient management.
authors.affiliation: Department of Pathology and Immunology.
authors.forename: Craig B
authors.initials: CB
authors.lastname: Wilen
authors.affiliation: Department of Pathology and Immunology.
authors.forename: Jeffrey J
authors.initials: JJ
authors.lastname: Szymanski
authors.affiliation: Department of Emergency Medicine, and.
authors.forename: Steven
authors.initials: S
authors.lastname: Hung
authors.affiliation: Department of Pathology and Immunology.
authors.forename: Anand
authors.initials: A
authors.lastname: Rajan
authors.affiliation: Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO.
authors.forename: Paul M
authors.initials: PM
authors.lastname: Lavigne
authors.affiliation: Department of Emergency Medicine, and.
authors.forename: Douglas M
authors.initials: DM
authors.lastname: Char
authors.affiliation: Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO.
authors.forename: Edward M
authors.initials: EM
authors.lastname: Geltman
authors.affiliation: Department of Pathology and Immunology, mscott@path.wustl.edu.
authors.forename: Mitchell G
authors.initials: MG
authors.lastname: Scott
mesh_terms: D000368:Aged; D001774:Blood Chemical Analysis / Q000379:methods*; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007902:Length of Stay; D057230:Limit of Detection; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis* / Q000628:therapy*; D017202:Myocardial Ischemia / Q000097:blood / Q000175:diagnosis / Q000628:therapy; D011237:Predictive Value of Tests; D012189:Retrospective Studies; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood*
chemical_list: D019210:Troponin I