title: Pathophysiology and prognostic significance of Holter-detected ST segment depression after myocardial infarction. The Tissue Plasminogen Activator: Toronto (TPAT) Study Group.
abstract: OBJECTIVE
  We performed Holter monitoring on days 4 and 7 after acute myocardial infarction in 109 patients to assess whether ST segment shift would identify those with more severe coronary artery disease, left ventricular dysfunction and unfavorable prognosis.
  
  
  BACKGROUND
  Silent myocardial ischemia is a frequent and prognostically significant event after acute myocardial infarction. However, the specific pathophysiologic mechanisms and the impact of thrombolytic therapy are uncertain.
  
  
  METHODS
  In addition to Holter monitoring, patients underwent exercise testing, radionuclide angiography on days 1 and 9 and quantitative coronary angiography on day 9.
  
  
  RESULTS
  Thirty-five patients (32%) had ST segment depression and had similar recombinant tissue-type plasminogen activator (rt-PA) treatment assignment and a reduced cross-sectional area of the infarct-related artery (0.59 +/- 0.57 vs. 1.04 +/- 1.26 mm2, p < 0.05). Global left ventricular function improved from day 1 to day 9 in patients without (4% +/- 11%, p < 0.001) but not in those with (0% +/- 7%) ST segment depression. In-hospital event rates were similar; however, follow-up 18 +/- 11 months after hospital discharge revealed a greater frequency of death and recurrent myocardial infarction in patients with compared with those without ST segment depression (27% vs. 6%, p = 0.03).
  
  
  CONCLUSIONS
  After acute myocardial infarction, approximately one third of patients have ST segment depression on Holter monitoring, independent of the use of thrombolytic therapy. The unfavorable prognosis observed in these patients may be related to greater lumen obstruction in the infarct-related artery and lack of improvement in left ventricular function.
authors.affiliation: St. Michael's Hospital, Toronto, Ontario, Canada.
authors.forename: A
authors.initials: A
authors.lastname: Langer
authors.forename: J
authors.initials: J
authors.lastname: Minkowitz
authors.forename: P
authors.initials: P
authors.lastname: Dorian
authors.forename: L
authors.initials: L
authors.lastname: Casella
authors.forename: L
authors.initials: L
authors.lastname: Harris
authors.forename: C D
authors.initials: CD
authors.lastname: Morgan
authors.forename: P W
authors.initials: PW
authors.lastname: Armstrong
mesh_terms: D006328:Cardiac Catheterization; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D004311:Double-Blind Method; D015716:Electrocardiography, Ambulatory / Q000706:statistics & numerical data; D005080:Exercise Test; D005500:Follow-Up Studies; D006801:Humans; D009203:Myocardial Infarction / Q000175:diagnosis / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology*; D011379:Prognosis; D011994:Recombinant Proteins / Q000627:therapeutic use; D012008:Recurrence; D015912:Thrombolytic Therapy / Q000706:statistics & numerical data; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D016277:Ventricular Function, Left
chemical_list: D011994:Recombinant Proteins; D010959:Tissue Plasminogen Activator