RELEASE KINETICS OF SERUM CARDIAC TROPONIN-I IN ISCHEMIC MYOCARDIAL INJURY

Objectives: The study was undertaken to evaluate the release kinetics of cardiac troponin I (cTn-I) in ischemic myocardial injury. Design an d Methods: The reference range for cTn-I was established by determinat ion 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) rec eiving intravenous thrombolysis (Group 3) (in this group, an additiona l 43 patients with MI were analyzed separately to characterize cTn-I p atterns in thrombolyzed and nonthrombolyzed populations); and in 44 pa tients with unstable angina (Group 4). Results: in Groups 1 and 2, no positive results (greater than or equal to 0.1 mu g/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-M B 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 disa ppeared significantly later in nonthrombolyzed than in the thrombolyze d group. In Group 4, positive tests results were detected in 45% of pa tients for cTn-I, 16% for CK-MB activity, and 32% for CK-MB mass. Conc lusions: The cTn-I assay appears to be ideally suited for the detectio n 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 ma ss in this respect.