title: Time course of degradation of cardiac troponin I in patients with acute ST-elevation myocardial infarction: the ASSENT-2 troponin substudy.
abstract: Although measurement of troponin is widely used for diagnosing acute myocardial infarction (AMI), its diagnostic potential may be increased by a more complete characterization of its molecular appearance and degradation in the blood. The aim of this study was to define the time course of cardiac troponin I (cTnI) degradation in patients with acute ST-elevation myocardial infarction (STEMI). In the ASSENT-2 substudy, 26 males hospitalized with STEMI were randomized to 2 different thrombolytic drugs within 6 hours after onset of symptoms. Blood samples were obtained just before initiation of thrombolysis and at 30 minutes intervals (7 samples per patient). Western blot analysis was performed using anti-cTnI antibodies and compared with serum concentrations of cTnI. All patients exceeded the cTnI cutoff for AMI during the sampling period; at initiation of therapy, 23 had elevated cTnI values. All patients demonstrated 2 bands on immunoblot: intact cTnI and a single degradation product as early as 90 minutes after onset of symptoms. On subsequent samples, 15 of 26 patients showed multiple degradation products with up to 7 degradation bands. The appearance of fragments was correlated with higher levels of cTnI (P<0.001) and time to initiation of treatment (P=0.058). This study defines for the first time the initial time course of cTnI degradation in STEMI. Intact cTnI and a single degradation product were detectable on immunoblot as early as 90 minutes after onset of symptoms with further degradation after 165 minutes. Infarct size and time to initiation of treatment was the major determinant for degradation.
authors.affiliation: Department of Cardiology and Endocrinology, Frederiksberg University Hospital, Copenhagen, Denmark. lhm@dadlnet.dk
authors.forename: Lene H
authors.initials: LH
authors.lastname: Madsen
authors.forename: Geir
authors.initials: G
authors.lastname: Christensen
authors.forename: Terje
authors.initials: T
authors.lastname: Lund
authors.forename: Victor L
authors.initials: VL
authors.lastname: Serebruany
authors.forename: Chris B
authors.initials: CB
authors.lastname: Granger
authors.forename: Ingvild
authors.initials: I
authors.lastname: Hoen
authors.forename: Zanina
authors.initials: Z
authors.lastname: Grieg
authors.forename: John H
authors.initials: JH
authors.lastname: Alexander
authors.forename: Allan S
authors.initials: AS
authors.lastname: Jaffe
authors.forename: Jennifer E
authors.initials: JE
authors.lastname: Van Eyk
authors.forename: Dan
authors.initials: D
authors.lastname: Atar
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000737:chemistry / Q000276:immunology; D015153:Blotting, Western; D004591:Electrophoresis, Polyacrylamide Gel; D000939:Epitopes / Q000032:analysis; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D047468:Immunoprecipitation; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy; D000077785:Tenecteplase; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D019210:Troponin I / Q000097:blood* / Q000276:immunology
chemical_list: D000911:Antibodies, Monoclonal; D000939:Epitopes; D005343:Fibrinolytic Agents; D019210:Troponin I; D010959:Tissue Plasminogen Activator; D000077785:Tenecteplase