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 (cTnI) in regard to predictive value and cardiac specificity is still ongoing.


METHODS
We evaluated enzyme-linked immunosorbent assay systems for cTnI 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, cTnI levels were below the detection limit of 0.2 microg/L and cTnT levels were 0.011 [0.010-0. 013] microg/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 cTnI, and 0.04 [0.01-0.10], 0.011 [0.005-0.025], and 0.032 [0.009-0.054] microg/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 microg/L for cTnI (29.0% positive) and at 0.06 microg/L for cTnT (35. 0% positive). Significant differences in the area-under-the-curve values were observed between cTnI 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. CTnI showed a less strong association with 30-day outcome than cTnT. When cTnI was put in a logistic multiple-regression model first, cTnT did add significant information.


CONCLUSIONS
By using the defined threshold values and the employed test systems, single testing for cTnI 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.
Heeschen
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C
Division of Cardiovascular Medicine, Stanford University School of Medicine, CA 94305-5406, USA. heeschen@stanford.edu
Deu
A
A
Langenbrink
L
L
Goldmann
B U
BU
Hamm
C W
CW
D000208:Acute Disease; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002637:Chest Pain / Q000097:blood; D003327:Coronary Disease / Q000097:blood* / Q000175:diagnosis; D004311:Double-Blind Method; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005500:Follow-Up Studies; D006493:Heparin / Q000494:pharmacology; D006801:Humans; D007231:Infant, Newborn; D007238:Infarction / Q000097:blood / Q000175:diagnosis; D008297:Male; D008875:Middle Aged; D015233:Models, Statistical; D015999:Multivariate Analysis; D018482:Muscle, Skeletal / Q000293:injuries; D020966:Muscular Disorders, Atrophic / Q000097:blood; D017202:Myocardial Ischemia / Q000097:blood / Q000175:diagnosis; D011237:Predictive Value of Tests; D011379:Prognosis; D011933:Reagent Kits, Diagnostic / Q000592:standards*; D012008:Recurrence; D051437:Renal Insufficiency / Q000097:blood; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity; D014336:Troponin / Q000097:blood*; D019210:Troponin I / Q000097:blood; D020107:Troponin T / Q000097:blood
D015415:Biomarkers; D011933:Reagent Kits, Diagnostic; D014336:Troponin; D019210:Troponin I; D020107:Troponin T; D006493:Heparin