title: Troponin T and quantitative ST-segment depression offer complementary prognostic information in the risk stratification of acute coronary syndrome patients.
abstract: OBJECTIVE
  Our primary objective was to examine the prognostic relationship between baseline quantitative ST-segment depression (ST) and cardiac troponin T (cTnT) elevation. The secondary objectives were to: 1) examine whether ST provided additional insight into therapeutic efficacy of glycoprotein IIb/IIIa therapy similar to that demonstrated by cTnT; and 2) explore whether the time to evaluation impacted on each marker's relative prognostic utility.
  
  
  BACKGROUND
  The relationship between the baseline electrocardiogram (ECG) and cTnT measurements in risk-stratifying patients presenting with acute coronary syndromes (ACS) has not been evaluated comprehensively.
  
  
  METHODS
  The study population consisted of 959 patients enrolled in the cTnT substudy of the Platelet IIb/IIIa Antagonism for the Reduction of Acute coronary syndrome events in a Global Organization Network (PARAGON)-B trial. Patients were classified as having no ST (n = 387), 1 mm ST (n = 433), and ST > or =2 mm (n = 139). Forty-percent (n = 381) were classified as cTnT-positive based on a definition of > or =0.1 ng/ml.
  
  
  RESULTS
  Six-month death/(re)myocardial infarction rates were 8.4% among cTnT-negative patients with no ST and 26.8% among cTnT-positive patients with ST > or =2 mm. On ECGs done after 6 h of symptom onset, ST > or =2 mm was associated with higher risk compared to its presence on ECGs done earlier (odds ratio [OR] 7.3 vs. 2.1). In contrast, the presence of elevated cTnT within 6 h of symptom was associated with a higher risk of adverse events compared with elevations after 6 h (OR 2.4 vs. 1.5).
  
  
  CONCLUSIONS
  Quantitative ST and cTnT status are complementary in assessing risk among ACS patients and both should be employed to determine prognosis and assist in medical decision making.
authors.affiliation: Duke Clinical Research Institute, Duke University, Durham, North Carolina, USA.
authors.forename: Padma
authors.initials: P
authors.lastname: Kaul
authors.forename: L Kristin
authors.initials: LK
authors.lastname: Newby
authors.forename: Yuling
authors.initials: Y
authors.lastname: Fu
authors.forename: Vic
authors.initials: V
authors.lastname: Hasselblad
authors.forename: Kenneth W
authors.initials: KW
authors.lastname: Mahaffey
authors.forename: Robert H
authors.initials: RH
authors.lastname: Christenson
authors.forename: Robert A
authors.initials: RA
authors.lastname: Harrington
authors.forename: E Magnus
authors.initials: EM
authors.lastname: Ohman
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Topol
authors.forename: Robert M
authors.initials: RM
authors.lastname: Califf
authors.forename: Frans
authors.initials: F
authors.lastname: Van de Werf
authors.forename: Paul W
authors.initials: PW
authors.lastname: Armstrong
mesh_terms: D000085:Acetates / Q000627:therapeutic use*; D000208:Acute Disease; D000368:Aged; D003327:Coronary Disease / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology*; D004562:Electrocardiography / Q000187:drug effects*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors* / Q000627:therapeutic use*; D011379:Prognosis; D018570:Risk Assessment; D013577:Syndrome; D013997:Time Factors; D020107:Troponin T / Q000097:blood* / Q000187:drug effects*; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000627:therapeutic use*
chemical_list: D000085:Acetates; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D020107:Troponin T; D014443:Tyrosine; C084062:lamifiban