Combined use of markers of muscle necrosis and fibrinogen conversion in the early differentiation of myocardial infarction and unstable angina.

14.5 mg/L; range, 6.9 –24.8 mg/L). No correlation was found between cTnI and ST-segment changes. Electrocardiograms showed ST-segment alteration in two patients with echocardiographic signs of MC and in two patients without MC signs. cTnI concentrations peaked between 6 and 12 h after chest trauma and disappeared 48–96 h after the trauma. Thus, the diagnostic window was narrower than it is during acute myocardial infarction, probably because of the lower peak serum concentration of cTnI. We conclude that: • The incidence of MC in our patients was 18%, as detected by TEE investigation. • All of the MC patients had a positive cTnI test (.0.4 mg/L). • The cTnI assay is more specific than CK-MB for MC after chest injury. The receiver operating characteristic curve shows the clinical performance of the two markers. Assuming that the cutoff concentrations for cTnI and CK-MB are 1.1 mg/L and 18 mg/L, respectively, these markers showed 100% (0.83– 1.0 mg/L) and 80% (0.56–0.95 mg/L) specificity (Fig. 1). • cTnI .1.1 mg/L indicates a cardiac lesion observable through TEE. Other authors have reported different cTnI cutoff concentrations that are .1.1 mg/L; the discrepancy is probably due to a different mode of echocardiographic investigation (6). • Serum cTnI concentrations of 0.4–1.1 mg/L could be indicative of microlesions of cardiac tissue not detectable by echocardiography.