title: Transient release of lipid peroxidation products as a non-invasive marker of successful reperfusion after thrombolysis for myocardial infarction.
abstract: OBJECTIVE
  To evaluate an increase in plasma concentration of thiobarbituric acid reactive substances as a non-invasive biochemical test of reperfusion after thrombolysis and to investigate the relation between the inflammatory response after acute myocardial infarction and the production of the substances.
  
  
  METHODS
  Venous samples were taken from 19 patients receiving thrombolysis for acute myocardial infarction before the start of therapy and every hour afterwards up to 5 hours and then at 24 and 48 hours and the concentration of thiobarbituric acid reactive substances measured. These substances are markers of lipid peroxidation induced by free oxygen radicals. Early reperfusion was judged by regression of ST elevation and late coronary artery patency from the results of coronary angiography 24-72 hours after thrombolysis.
  
  
  RESULTS
  The concentration of thiobarbituric acid reactive substances increased in only 6 out of 14 patients with signs of early reperfusion. In patients with late coronary artery patency the corresponding number was 6 out of 15. However, a significant increase in the concentration of thiobarbituric acid reactive substances was found for the whole group 24 and 48 hours after treatment. The change in concentration in serum correlated significantly with that of C reactive protein--an acute phase reactant (r = 0.62, P < 0.01)--but not to the serum activities of markers of infarct size such as creatine kinase B and lactate dehydrogenase.
  
  
  CONCLUSIONS
  The fluorimetric assay used in this study to measure the concentration of thiobarbituric acid reactive substances seems to be an insensitive method of detecting reperfusion after thrombolysis for myocardial infarction. The increase in concentrations found 24 and 48 hours after treatment correlated with C reactive protein concentrations but not with those of markers of infarct size.
authors.affiliation: Department of Medicine, University Hospital, Lund, Sweden.
authors.forename: H
authors.initials: H
authors.lastname: Ohlin
authors.forename: C G
authors.initials: CG
authors.lastname: Gustavsson
authors.forename: E
authors.initials: E
authors.lastname: Pantev
authors.forename: B
authors.initials: B
authors.lastname: Thorvinger
authors.forename: A K
authors.initials: AK
authors.lastname: Ohlin
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D017023:Coronary Angiography; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000097:blood; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000201:enzymology; D015425:Myocardial Reperfusion; D013300:Streptokinase / Q000627:therapeutic use*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism*; D015912:Thrombolytic Therapy; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D017392:Thiobarbituric Acid Reactive Substances; D002097:C-Reactive Protein; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D013300:Streptokinase