title: Quantitative troponin and death, cardiogenic shock, cardiac arrest and new heart failure in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS): insights from the Global Registry of Acute Coronary Events.
abstract: BACKGROUND
  The objective of this study was to determine if the extent of quantitative troponin elevation predicted mortality as well as in-hospital complications of cardiac arrest, new heart failure and cardiogenic shock.
  
  
  METHODS
  16,318 patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS) from the Global Registry of Acute Coronary Events (GRACE) were included. The maximum 24 h troponin value as a multiple of the local laboratory upper limit of normal was used. The population was divided into five groups based on the degree of troponin elevation, and outcomes were compared. An adjusted analysis was performed using quantitative troponin as a continuous variable with adjustment for known prognostic variables.
  
  
  RESULTS
  For each approximate 10-fold increase in the troponin ratio, there was an associated increase in cardiac arrest, sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) (1.0, 2.4, 3.4, 5.9 and 13.4%; p<0.001 for linear trend), cardiogenic shock (0.5, 1.4, 2.0, 4.4 and 12.7%; p<0.001), new heart failure (2.5, 5.1, 7.4, 11.6 and 15.8%; p<0.001) and mortality (0.8, 2.2, 3.0, 5.3 and 14.0%; p<0.001). These findings were replicated using the troponin ratio as a continuous variable and adjusting for covariates (cardiac arrest, sustained VT or VF, OR 1.56, 95% CI 1.39 to 1.74; cardiogenic shock, OR 1.87, 95% CI 1.61 to 2.18; and new heart failure, OR 1.57, 95% CI 1.45 to 1.71). The degree of troponin elevation was predictive of early mortality (HR 1.61, 95% CI 1.44 to 1.81; p<0.001 for days 0-14) and longer term mortality (HR 1.18, 95% CI 1.07 to 1.30, p=0.001 for days 15-180).
  
  
  CONCLUSIONS
  The extent of troponin elevation is an independent predictor of morbidity and mortality.
authors.affiliation: Population Health Research Institute, Department of Medicine, Hamilton Health Sciences, McMaster University, Hamilton, Ontario, Canada. jollyss@mcmaster.ca
authors.forename: Sanjit S
authors.initials: SS
authors.lastname: Jolly
authors.forename: Heather
authors.initials: H
authors.lastname: Shenkman
authors.forename: David
authors.initials: D
authors.lastname: Brieger
authors.forename: Keith A
authors.initials: KA
authors.lastname: Fox
authors.forename: Andrew T
authors.initials: AT
authors.lastname: Yan
authors.forename: Kim A
authors.initials: KA
authors.lastname: Eagle
authors.forename: P Gabriel
authors.initials: PG
authors.lastname: Steg
authors.forename: Ki-Dong
authors.initials: KD
authors.lastname: Lim
authors.forename: Ann
authors.initials: A
authors.lastname: Quill
authors.forename: Shaun G
authors.initials: SG
authors.lastname: Goodman
mesh_terms: D054058:Acute Coronary Syndrome / Q000150:complications / Q000175:diagnosis* / Q000401:mortality; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D004562:Electrocardiography; D004812:Epidemiologic Methods; D005260:Female; D006323:Heart Arrest / Q000453:epidemiology / Q000209:etiology; D006333:Heart Failure / Q000453:epidemiology / Q000209:etiology; D006760:Hospitalization; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology; D011379:Prognosis; D012008:Recurrence; D012770:Shock, Cardiogenic / Q000453:epidemiology / Q000209:etiology; D019210:Troponin I / Q000097:blood*; D020107:Troponin T / Q000097:blood*
chemical_list: D015415:Biomarkers; D019210:Troponin I; D020107:Troponin T