title: Release kinetics of serum cardiac troponin I in ischemic myocardial injury.
abstract: OBJECTIVE
  The study was undertaken to evaluate the release kinetics of cardiac troponin I (cTn-I) in ischemic myocardial injury.
  
  
  METHODS
  The reference range for cTn-I was established by determination of cTn-I in sera and plasma obtained from 622 healthy volunteers (Group 1). cTn-I was compared to: (a) Creatine kinase (CK) MB mass and myoglobin in 12 patients with severe skeletal muscle damage (Group 2); (b) CK-MB activity in 48 patients with myocardial infarction (MI) receiving intravenous thrombolysis (Group 3) (in this group, an additional 43 patients with MI were analyzed separately to characterize cTn-I patterns in thrombolyzed and nonthrombolyzed populations): and in 44 patients with unstable angina (Group 4).
  
  
  RESULTS
  In Groups 1 and 2, no positive results (> or = 0.1 microgram/L) were obtained. In Group 3, the time-courses of cTn-I were mostly monophasic in form. A pathologic increase occurred earlier in cTn-I than in CK-MB activity (p = 0.0002); the period with increased cTn-I was longer (p = 0.001), the overall sensitivity of cTn-I (93.9%) was higher than that of CK-MB activity (p = 0.00001). cTn-I was more sensitive at admission (p = 0.0004). In additional patients, the cTn-I peak occurred and cTn-I disappeared significantly later in nonthrombolyzed than in the thrombolyzed group. In Group 4, positive tests results were detected in 45% of patients for cTn-I, 16% for CK-MB activity, and 32% for CK-MB mass.
  
  
  CONCLUSIONS
  The cTn-I assay appears to be ideally suited for the detection of ischemic myocardial injury in complex clinical situations because of its high specificity; cTn-I indicates myocardial tissue damage in patients with unstable angina and is superior to CK-MB activity and mass in this respect.
authors.affiliation: Department of Cardiology, University Hospital of Nîmes, France.
authors.forename: J P
authors.initials: JP
authors.lastname: Bertinchant
authors.forename: C
authors.initials: C
authors.lastname: Larue
authors.forename: I
authors.initials: I
authors.lastname: Pernel
authors.forename: B
authors.initials: B
authors.lastname: Ledermann
authors.forename: P
authors.initials: P
authors.lastname: Fabbro-Peray
authors.forename: L
authors.initials: L
authors.lastname: Beck
authors.forename: C
authors.initials: C
authors.lastname: Calzolari
authors.forename: S
authors.initials: S
authors.lastname: Trinquier
authors.forename: J
authors.initials: J
authors.lastname: Nigond
authors.forename: B
authors.initials: B
authors.lastname: Pau
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000789:Angina, Unstable / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D006801:Humans; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis / Q000188:drug therapy; D009211:Myoglobin / Q000097:blood; D011994:Recombinant Proteins / Q000627:therapeutic use; D013300:Streptokinase / Q000627:therapeutic use; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D019210:Troponin I / Q000097:blood*
chemical_list: D009211:Myoglobin; D011994:Recombinant Proteins; D019210:Troponin I; D003402:Creatine Kinase; D013300:Streptokinase; D010959:Tissue Plasminogen Activator