title: Comparative prognostic significance of simultaneous versus independent resolution of ST segment depression relative to ST segment elevation during acute myocardial infarction.
abstract: OBJECTIVE
  We sought to determine the prognostic significance of simultaneous versus independent resolution of ST segment depression that occurs concomitant with ST segment elevation during acute myocardial infarction (AMI).
  
  
  BACKGROUND
  ST segment depression in leads other than those showing ST segment elevation during AMI is a common phenomenon. Whether this indicates adverse outcomes remains controversial. We hypothesized that the timing of ST segment depression resolution relative to ST segment elevation resolution might differentiate between a high risk group and a low risk group of patients.
  
  
  METHODS
  Continuous 12-lead ST segment monitoring was performed after thrombolytic therapy for AMI in 413 patients, 261 of whom met technical criteria for analysis. Blinded analysis of ST segment depression resolution patterns was used to group patients as follows: 1) no ST segment depression at any time (control group); 2) ST segment depression resolving simultaneously with ST segment elevation (simultaneous group); and 3) ST segment depression persisting after ST segment elevation resolution (independent group). These patterns were correlated with the outcomes-recurrent angina, reinfarction, heart failure and death-using chi-square analysis and the Fisher exact test for categoric variables and the Wilcoxon rank-sum test for continuous variables.
  
  
  RESULTS
  The incidence of recurrent angina, reinfarction and heart failure was similar among the three groups. In-hospital mortality, however, was significantly higher in the independent group (13%) than either the simultaneous group (1%, p < 0.001) or the control group (0%, p = 0.002).
  
  
  CONCLUSIONS
  Continuous analysis of ST segment resolution identifies, among patients with AMI with concomitantly occurring ST segment elevation and depression, a subgroup with increased in-hospital mortality. The pathogenic mechanism of increased mortality is not currently known.
authors.affiliation: Division of Cardiology, Duke University Medical Center, Durham, North Carolina 27710, USA. wagne004@mc.duke.edu
authors.forename: A
authors.initials: A
authors.lastname: Shah
authors.forename: G S
authors.initials: GS
authors.lastname: Wagner
authors.forename: R M
authors.initials: RM
authors.lastname: Califf
authors.forename: R E
authors.initials: RE
authors.lastname: Boineau
authors.forename: C L
authors.initials: CL
authors.lastname: Green
authors.forename: N M
authors.initials: NM
authors.lastname: Wildermann
authors.forename: K M
authors.initials: KM
authors.lastname: Trollinger
authors.forename: J E
authors.initials: JE
authors.lastname: Pope
authors.forename: M W
authors.initials: MW
authors.lastname: Krucoff
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000209:etiology; D004562:Electrocardiography; D005260:Female; D006333:Heart Failure / Q000209:etiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000175:diagnosis / Q000401:mortality / Q000503:physiopathology*; D011379:Prognosis