title: Differential free-radical activity after successful and unsuccessful thrombolytic reperfusion in acute myocardial infarction.
abstract: BACKGROUND
  Free-radical generation after successful thrombolysis in acute myocardial infarction may jeopardize ischaemic but viable myocardium, thus limiting the optimal benefits of reperfusion.
  
  
  METHODS
  Circulating free-radical activity was assessed in 25 consecutive patients with acute myocardial infarction. Those who successfully reperfused (Group A) were compared with those who did not (Group B). We also compared patients who had or had not developed Q waves and patients with and without previous angina or myocardial infarction. All patients presented within 6 h of the onset of chest pain and received standard intravenous streptokinase therapy. Free-radical activity in serial serum samples collected over 72 h was measured using the percentage molar ratio (PMR) of the concentrations of 9,11-linoleic acid to 9,12-linoleic acid, and malonaldehyde concentration.
  
  
  RESULTS
  Throughout the study period Group A (n = 11) showed significantly greater change in serum PMR and malonaldehyde levels compared with Group B (n = 14) (P < 0.01). PMR differences between the two groups were most pronounced at 3 and 12 h (P < 0.001). Patients with non-Q-wave myocardial infarction (n = 5) showed significantly greater changes in serum PMR and malonaldehyde levels (P < 0.01) compared with those with Q-wave infarction (n = 20). A history of previous infarction or angina had no apparent effects on the changes in serum free-radical activity.
  
  
  CONCLUSIONS
  Successful early reperfusion and non-Q-wave myocardial infarction are both associated with a significantly greater increase in the levels of markers of serum free-radical activity immediately after infarction. The results support present concepts of free-radical-mediated reperfusion injury. Use of these assays may identify those patients who may be at risk from free-radical-mediated reperfusion injury.
authors.affiliation: Department of Cardiology, Cardiothoracic Centre, Liverpool, UK.
authors.forename: E D
authors.initials: ED
authors.lastname: Grech
authors.forename: C I
authors.initials: CI
authors.lastname: Jack
authors.forename: C
authors.initials: C
authors.lastname: Bleasdale
authors.forename: M J
authors.initials: MJ
authors.lastname: Jackson
authors.forename: M
authors.initials: M
authors.lastname: Baines
authors.forename: E B
authors.initials: EB
authors.lastname: Faragher
authors.forename: C R
authors.initials: CR
authors.lastname: Hind
authors.forename: R A
authors.initials: RA
authors.lastname: Perry
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D005260:Female; D005609:Free Radicals / Q000009:adverse effects / Q000097:blood; D006801:Humans; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000097:blood; D044243:Linoleic Acids, Conjugated; D008297:Male; D008315:Malondialdehyde / Q000097:blood*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000097:blood* / Q000209:etiology; D015912:Thrombolytic Therapy; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D005609:Free Radicals; D008041:Linoleic Acids; D044243:Linoleic Acids, Conjugated; C046938:9,11-linoleic acid; D008315:Malondialdehyde; D019787:Linoleic Acid