title: Thrombolytic therapy does not change the release ratios of enzymatic and non-enzymatic myocardial marker proteins.
abstract: Measurements of cardiac marker proteins in plasma from patients with acute myocardial infarction (AMI) have become important in the evaluation of recanalization therapy. The validity of this approach has however been questioned, because it was claimed that coronary reperfusion may increase the recovery in plasma of cardiac enzymes, such as creatine kinase (CK). In the present study, possible effects of thrombolytic therapy on the release of enzymatic and nonenzymatic marker proteins were investigated. Activities of CK and lactate dehydrogenase (LDH), and concentrations of myoglobin (Mb) and fatty acid-binding protein (FABP) were determined in serial plasma samples obtained from 50 patients with confirmed AMI, of whom 36 received thrombolytic therapy, and 14 did not. Treatment delay was 2.8+/-1.6 (mean+/-SD) h, and hospital delay in untreated patients was 2.7+/-1.8 h. Average infarct size, expressed in gram-equivalents of heart muscle per litre of plasma (g-eq/l), varied between 5.5 and 7.2 g-eq/l for the four marker proteins in patients treated with thrombolytic therapy, and between 4.6 and 6.4 g-eq/l in untreated patients, with a tendency to larger infarct sizes for Mb and FABP than for CK and LDH. Thrombolytic therapy, although significantly accelerating protein release rates, did not influence the release ratios. These results indicate that thrombolytic therapy has no significant effects on the recovery of cardiac marker proteins in plasma.
authors.affiliation: Department of Clinical Chemistry, Academic Hospital Maastricht, The Netherlands.
authors.forename: K W
authors.initials: KW
authors.lastname: Wodzig
authors.forename: J A
authors.initials: JA
authors.lastname: Kragten
authors.forename: W
authors.initials: W
authors.lastname: Modrzejewski
authors.forename: J
authors.initials: J
authors.lastname: Górski
authors.forename: M P
authors.initials: MP
authors.lastname: van Dieijen-Visser
authors.forename: J F
authors.initials: JF
authors.lastname: Glatz
authors.forename: W T
authors.initials: WT
authors.lastname: Hermens
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002352:Carrier Proteins / Q000097:blood* / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood*; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D005227:Fatty Acids / Q000378:metabolism; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000097:blood*; D008875:Middle Aged; D018996:Myelin P2 Protein / Q000097:blood* / Q000378:metabolism; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D009211:Myoglobin / Q000097:blood*; D009363:Neoplasm Proteins; D015912:Thrombolytic Therapy; D025521:Tumor Suppressor Proteins
chemical_list: D015415:Biomarkers; D002352:Carrier Proteins; C107608:FABP7 protein, human; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D005227:Fatty Acids; D018996:Myelin P2 Protein; D009211:Myoglobin; D009363:Neoplasm Proteins; D025521:Tumor Suppressor Proteins; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase