CARDIAC TROPONIN-I IN THE DIAGNOSIS OF MYOCARDIAL INJURY AND INFARCTION

We used a cardiospecific enzymoimmunometric assay to measure cardiac t roponin I (cTnI) in samples serially drawn from 78 patients with acute myocardial infarction (AMI), 7 patients with unstable angina (Braunwa ld class III), 22 multi-traumatized patients, and in 30 athletes after eccentric exercise, as well as in 101 non-traumatic chest pain patien ts on admission to the emergency department, cTnI assay crossreactivit y with crude human skeletal muscle homogenates was <0.1%. cTnI could n ot 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 an d mostly peaked parallel to cTnI, cTnT sensitivity on the 7th day afte r 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 thr ombolytic 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 biochemical markers f or early AMI diagnosis in non-traumatic chest pain patients on admissi on, with CKMB mass showing the highest value (0.76). Our results demon strate that cTnI is a highly sensitive and specific marker for myocard ial damage which is suitable for early and late diagnosis.