title: Cardiac troponin I in the diagnosis of myocardial injury and infarction.
abstract: We used a cardiospecific enzymoimmunometric assay to measure cardiac troponin I (cTnI) in samples serially drawn from 78 patients with acute myocardial infarction (AMI), 7 patients with unstable angina (Braunwald class III), 22 multi-traumatized patients, and in 30 athletes after eccentric exercise, as well as in 101 non-traumatic chest pain patients on admission to the emergency department. cTnI assay crossreactivity with crude human skeletal muscle homogenates was < 0.1%. cTnI could not be detected in athletes or multi-traumatized patients except for 2 trauma patients with myocardial damage. Increased cTnI concentrations were found in 6 of 7 patients with unstable angina at rest and in all AMI patients. After AMI, cTnI increased about 3.5 h (median) after the onset of chest pain, reached peak values parallel to CKMB, and stayed increased for at least 4 days. Cardiac troponin T (cTnT) increased and mostly peaked parallel to cTnI. cTnT sensitivity on the 7th day after AMI was significantly higher than that of cTnI. In contrast to cTnI, cTnT mostly showed a second, usually smaller, peak about day 4 after AMI. During the first 4 h after the onset of chest pain and before thrombolytic therapy the sensitivities of myoglobin (0.43) and CKMB mass (0.56) were significantly higher than those of both troponins (cTnI, 0.29; cTnT, 0.25). Areas under receiver operator characteristic curves indicated only moderate diagnostic accuracies of bio-chemical markers for early AMI diagnosis in non-traumatic chest pain patients that cTnI is a highly sensitive and specific marker for myocardial damage which is suitable for early and late diagnosis.
authors.affiliation: Department of Medical Chemistry, University of Innsbruck Medical School, Austria.
authors.forename: J
authors.initials: J
authors.lastname: Mair
authors.forename: N
authors.initials: N
authors.lastname: Genser
authors.forename: D
authors.initials: D
authors.lastname: Morandell
authors.forename: J
authors.initials: J
authors.lastname: Maier
authors.forename: P
authors.initials: P
authors.lastname: Mair
authors.forename: P
authors.initials: P
authors.lastname: Lechleitner
authors.forename: C
authors.initials: C
authors.lastname: Calzolari
authors.forename: C
authors.initials: C
authors.lastname: Larue
authors.forename: E
authors.initials: E
authors.lastname: Ambach
authors.forename: F
authors.initials: F
authors.lastname: Dienstl
authors.forename: B
authors.initials: B
authors.lastname: Pau
authors.forename: B
authors.initials: B
authors.lastname: Puschendorf
mesh_terms: D000328:Adult; D000368:Aged; D015444:Exercise; D005260:Female; D006335:Heart Injuries / Q000175:diagnosis* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D012680:Sensitivity and Specificity; D015912:Thrombolytic Therapy; D014336:Troponin / Q000097:blood*; D019210:Troponin I
chemical_list: D014336:Troponin; D019210:Troponin I