Comparison of serum cardiac specific troponin-I with creatine kinase, creatine kinase-MB isoenzyme, tropomyosin, myoglobin and C-reactive protein release in marathon runners: cardiac or skeletal muscle trauma?

Problems arise in distinguishing skeletal from cardiac muscle trauma on the basis of serum enzyme tests following severe muscle exercise. The contributions of cardiac and skeletal sources have been assessed in eleven marathon runners by measuring pre- and post-race serum levels of cardiac-specific myofibrillar troponin-I together with total creatine kinase, creatine kinase-MB isoenzyme, myoglobin, myofibrillar tropomyosin and C-reactive protein. Total creatine kinase, creatine kinase-MB isoenzyme, tropomyosin and myoglobin were significantly elevated above pre-race levels in all runners between 1 h and 128 h post-race. Neither mean cardiac troponin-I nor C-reactive protein was elevated post-race. Nine out of sixty-three samples fulfilled conventional positive criteria for cardiac muscle damage on the basis of combined creatine kinase and creatine kinase-MB isoenzyme levels. Six runners had one or more positive samples. No samples had levels above twice the upper normal limit for either cardiac troponin-I or C-reactive protein. Correlation analysis of levels in each sample indicated skeletal and not cardiac muscle as the source of raised serum protein.

Cardiac-specific troponin-I radioimmunoassay in the diagnosis of acute myocardial infarction.

The cardiac isotype of the myofibrillar contractile protein, troponin-I, is located specifically in the mammalian heart. A sensitive radioimmunoassay has been developed to detect human and nonhuman primate cardiac troponin-I in serum down to 10 ng/ml. Immunochemical cross reactivity with skeletal troponin-I was only 2% and was species nonspecific. Normal patient levels of cardiac troponin-I are about 10 ng/ml. In patients with acute myocardial infarction (n = 32), serum cardiac troponin-I was elevated within 4 to 6 hours, reached a mean peak level of 112 ng/ml (range 20 to 550 ng/ml) at 18 hours, and remained above normal for up to 6 to 8 days following infarction. Peak cardiac troponin-I correlated with peak creatine kinase (CK) MB isoenzyme (r = 0.75). In subjects (n = 34) with skeletal muscle damage (total CK = 338 to 5384 IU/L), cardiac troponin-I levels were not elevated above normal, although CK-MB isoenzyme was elevated in some patients. Cardiac troponin-I levels were normal or slightly elevated in patients with ischemic heart disease and were normal in patients with chest pain of noncardiac origin. Immunoassay of cardiac troponin-I could be a valuable diagnostic aid in the cardiac-specific detection of cell necrosis.