Analytical and diagnostic performance of troponin assays in patients suspicious for acute coronary syndromes

Background: The controversy whether there is a clinically significant difference between troponin T (cTnT) and troponin I (cTnl) in regard to predictive value and cardiac specificity is still ongoing. Methods: We evaluated enzyme-linked immunosorbent assay systems for cTnl and cTnT in patients with acute coronary syndromes and multiple control groups to define threshold values for risk stratification and compare their predictive value. Results: In 312 patients with noncardiac chest pain, cTnl levels were below the detection limit of 0.2 mu g/L and cTnT levels were 0.011 [0.010-0.013] mu g/L. In patients with end-stage renal failure (n = 26) and acute (n = 38) or chronic (n =16) skeletal muscle damage, median concentrations were 0.20 [0.20-0.35], below the detection limit, and 0.20 [0.20-0.25] for cTnl, and 0.04 [0.01-0.10], 0.011 [0.005-0.025], and 0.032 [0.009-0.054] mu g/L for cTnT. In patients with acute coronary syndromes (n = 1130), maximized prognostic value for 30-day outcome (death, infarction) was observed at a threshold level of 1.0 mu g/L for cTnl (29.0% positive) and at 0.06 mu g/L for cTnT (35.0% positive). Significant differences in the area-under-the-curve values were observed between cTnl and cTnT (0.685 vs. 0.802; p = 0.005). For both markers, the area-under-the-curve values did not increase with the second (within 24 h after enrollment) or third (48 h) blood draw. CTnl showed a less strong association with 30-day outcome than cTnT. When cTnl was put in a logistic multiple-regression model first, cTnT did add significant information. Conclusion: By using the defined threshold values and the employed test systems, single testing for cTnl and cTnT within 12 h after symptom onset was appropriate for risk stratification. Despite the lower cardiac specificity for cTnT, it appears to have a stronger association with the patients' outcome, whereas, as previously shown, the ability to identify patients who benefit from treatment with a GP IIb/IIIa receptor antagonist is similar. Copyright (C) 2000 The Canadian Society of Clinical Chemists.