title: The prognostic and therapeutic implications of increased troponin T levels and ST depression in unstable coronary artery disease: the FRISC II invasive troponin T electrocardiogram substudy.
abstract: BACKGROUND
  In unstable coronary artery disease, both increased troponin T level and occurrence of ST-segment depression are associated with a worse prognosis. In the Fast Revascularisation in InStability in Coronary disease trial II invasive study, we evaluated whether the troponin T level, alone and combined with ST depression, identified more severe coronary artery disease or a greater efficacy of an early invasive strategy.
  
  
  METHODS
  In the study, 2457 patients with unstable coronary artery disease were randomized to early invasive or noninvasive strategy. Troponin T value and admission electrocardiogram results were available in 2286 patients.
  
  
  RESULTS
  In the noninvasive cohort, death or myocardial infarction occurred in 16.6% with troponin T level > or =0.03 microg/L versus 8.5% with troponin T level < 0.03 microg/L (P <.001). In the invasive group, 49% of patients with both ST depression and troponin T level > or =0.03 microg/L had 3-vessel or left main disease compared with 17% if neither finding was present (P <.001). The invasive strategy reduced death/myocardial infarction at 12 months in the cohort with both ST depression and troponin T level > or =0.03 microg/L from 22.1% to 13.2% (risk ratio, 0.60; 95% confidence interval, 0.43 to 0.82; P =.001). In the cohort with either ST depression or troponin T level > or =0.03 microg/L or neither of these findings, the absolute gain of the invasive strategy was smaller and more uncertain.
  
  
  CONCLUSIONS
  Patients with unstable coronary artery disease with the combination of troponin T level > or =0.03 microg/L and ST depression have a poor prognosis and, in half of the cases, 3-vessel or left main disease. In these patients, an early invasive strategy will substantially reduce death/myocardial infarction.
authors.affiliation: Department of Cardiology, University Hospital, Uppsala, Sweden. erik.diderholm@card.uas.lul.se
authors.forename: Erik
authors.initials: E
authors.lastname: Diderholm
authors.forename: Bertil
authors.initials: B
authors.lastname: Andrén
authors.forename: Gunnar
authors.initials: G
authors.lastname: Frostfeldt
authors.forename: Margareta
authors.initials: M
authors.lastname: Genberg
authors.forename: Tomas
authors.initials: T
authors.lastname: Jernberg
authors.forename: Bo
authors.initials: B
authors.lastname: Lagerqvist
authors.forename: Bertil
authors.initials: B
authors.lastname: Lindahl
authors.forename: Per
authors.initials: P
authors.lastname: Venge
authors.forename: Lars
authors.initials: L
authors.lastname: Wallentin
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D015331:Cohort Studies; D016001:Confidence Intervals; D003327:Coronary Disease / Q000097:blood* / Q000503:physiopathology* / Q000628:therapy; D017985:Dalteparin / Q000627:therapeutic use; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000401:mortality; D011379:Prognosis; D012044:Regression Analysis; D020107:Troponin T / Q000097:blood*
chemical_list: D015415:Biomarkers; D020107:Troponin T; D017985:Dalteparin