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Letters to the Editor |
1 Interventionelle Kardiologie Spandau, Berlin, Germany
2 Deutsches Herzzentrum Berlin, Berlin, Germany
3 Medizinische Klinik (Kardiologie), Charité–Universitätsmedizin Berlin (CCM), Berlin, German
4 Cardiovascular Division, and, Division of Laboratory Medicine, Mayo Medical School, Rochester, MN
aAddress correspondence to this author at: Interventionelle Kardiologie Spandau, Neuendorfer Str. 70, 13585 Berlin, Germany. Fax 49-30-3039-8029; e-mail oschulz{at}cath-lab-spandau.de.
To the Editor:
Recent studies, including outcome data (1), suggest that troponin values below the 99th percentile contain important diagnostic information. We reported that patients with stable chronic heart failure have cardiac troponin I (cTnI) values below the 99th percentile but above the detection limit (2), whereas in control individuals, cTnI is usually undetectable. Recently, we asked whether values below the 99th percentile were helpful in distinguishing patients with more severe heart disease from those with less severe disease. We studied 146 consecutive stable cardiovascular outpatients scheduled for cardiac catheterization [88 males; mean (SD) age, 64 (8) years] with bicycle stress tests, echocardiography, and left heart catheterization. After catheterization, without knowledge of the cTnI values, the patients were divided into those with (a) coronary artery disease [CAD; n = 80 (55%)], i.e., patients with at least one coronary artery stenosis 
70%; (b) myocardial dysfunction [MyD; n = 24 (17%)], i.e., patients with abnormal systolic or diastolic function, volume, or pressure load attributable to valvular heart disease; or (c) patients lacking the characteristics of the CAD or MyD groups (n = 42; 29%).
Plasma samples (lithium heparin) were obtained before catheterization. cTnI was measured by the second-generation Stratus CS® with reagents provided by Dade Behring. The limit of detection for this assay is 0.02 µg/L (3), the 99th percentile is 0.07 µg/L (4)(5), and the lowest concentration with a CV <10% has been reported as both 0.06 µg/L (5) and 0.10 µg/L(4), respectively. Measurements were performed in duplicate and averaged if within 3 SD of the variance of the assay, estimated to be 20%. If values were more discrepant, a third value was done, and they were averaged.
cTnI results for the 3 groups and for a combined CAD and/or MyD group are shown in Fig. 1
. In those with CAD or MyD, cTnI was detectable in 69.2% of patients and undetectable in the remainder. In the control group (Con), cTnI was detectable in 26.2% and undetectable in 73.8% of the patients. Of the detectable values, 87.5% were 
0.07 µg/L (the 99th percentile value) in the CAD and MyD groups; the remainder were between 0.07 and 0.1 µg/L (8.3%) or >0.1 µg/L (4.2%). In the control group, all detectable values were 0.07 µg/L. The ROC curve analysis suggested that a cTnI cutoff concentration of 0.02 µg/L best distinguished persons with ischemic (CAD) or nonischemic (MyD) myocardial impairment (area under the curve, 0.74; 95% confidence interval, 0.66–0.83) from those with milder disease. Regression analysis showed that the only variable that correlated with cTnI was left ventricular ejection fraction (r2 = 0.097; r = –0.311; P <0.001). In all 12 patients with an ejection fraction <50%, cTnI concentrations were detectable [median (75th–25th percentiles), 0.045 (0.0275–0.06) µg/L].
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Our data suggest a difference in cTnI concentrations between groups of cardiovascular outpatients with more severe disease compared with less severely affected patients. These differences are all below the 99th percentile of a reference interval. The mechanisms responsible for measurable cTnI values of this type are unclear. The group data are intriguing and suggest that when better assays permit evaluation of low values, there appears to be additional information that can be used to evaluate patients.
References
The following articles in journals at HighWire Press have cited this article:
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  A. E. Arai False positive or true positive troponin in patients presenting with chest pain but 'normal' coronary arteries: lessons from cardiac MRI Eur. Heart J., May 2, 2007; 28(10): 1175 - 1177. [Full Text] [PDF]
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 P. A. Kavsak, A. M. Newman, V. Lustig, A. R. MacRae, G. E. Palomaki, D. T. Ko, J. V. Tu, and A. S. Jaffe Long-Term Health Outcomes Associated with Detectable Troponin I Concentrations Clin. Chem., February 1, 2007; 53(2): 220 - 227. [Abstract] [Full Text] [PDF]
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 A. S. Jaffe Chasing Troponin: How Low Can You Go if You Can See the Rise? J. Am. Coll. Cardiol., November 7, 2006; 48(9): 1763 - 1764. [Full Text] [PDF]
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