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1 Departments of Internal Medicine, Division of Cardiovascular Diseases, and Laboratory Medicine and Pathology, Mayo Clinic and Mayo Medical School, Rochester, MN
2 Abteilung Innere Medizin III, Medizinische Klinik, Universitätsklinikum Heidelberg, Heidelberg, Germany
aAddress correspondence to this author at: Mayo Clinic, 200 First St SW, Division of Cardiovascular Diseases, Gonda 5, Rochester, MN 55905, Fax 507-266-0228, e-mail Jaffe.Allan{at}mayo.edu
To the Editor:
The extent of myocardial infarction (MI) is related to patient outcomes (1), and clinicians often wish to have a sense for this critical measure. Imaging methods, although accurate, have limited accessibility and high cost. Thus clinicians often use biomarkers to provide such an estimate. Measurement of cardiac troponin T (cTnT) at 96 h after onset of MI was observed to correlate with MRI-determined infarct size in both ST-elevation MI (STEMI) and non-STEMI (2). We tested the hypothesis that cardiac troponin I (cTnI), another myocardium-specific biomarker, would provide an equivalent estimation in the subset of STEMI patients previously described (2).
The 28 patients with STEMI had sufficient sample remaining to allow for determination of cTnI (2). The characteristics of this group have previously been reported (2), but in brief the mean age (SD) was 56 (11) years, and 17.4% of patients were women. Mean (SD) body mass index was 26.46 (3.5) kg/m2, and 71.4% of patients were hypertensive, 64.3% were current smokers, 60.7% had hypercholesterolemia, and 14.3% had diabetes. Blood samples were available at admission and at 24, 48, 72, and 96 h after onset of symptoms. cTnI concentrations were measured at a laboratory in Heidelberg, Germany, with the AccuTnI assay (Beckman-Coulter). The assay has a limit of detection of 0.01 µg/L, with a 99th percentile as low as 0.02–0.03 µg/L. In the laboratory performing the measurements, a cutoff value of 0.03 µg/L was used. Cardiac MRI was performed as described elsewhere (2). Plasma concentrations of cTnI are reported as median with the corresponding interquartile range (IQR). For all analyses, a value of P <0.05 was considered statistically significant. Correlation coefficients were calculated by the Spearman test.
Of the 28 study patients with STEMI, 7.1% of patients (2 of 28) received fibrinolytic agents before percutaneous coronary intervention; the remainder underwent primary percutaneous coronary intervention. Preinterventional thrombolysis in myocardial infarction flow grade 3 was present in 12 of 28 patients (42.3%) before PCI and in 27 of 28 patients (96.4%) after. The median time delay from onset of symptoms to balloon angioplasty was 6.25 h. MRI was performed at median of 4 days (range 3–4 days). All patients manifested delayed hyperenhancement observed with MRI; in 60.71% of patients (17 of 28) hyperenhancement was transmural. Mean infarct size relative to heart weight was 18.2% (IQR 7%–49%). Ventricular function evaluated by MRI revealed a mean ejection fraction of 54.4% (27.9%–63.6%) and a mean stroke volume of 91.32 mL (42.4–109.3 mL). The median absolute value for infarct size was 29.3 g (IQR 16.6–53.0 g). Spearman analysis demonstrated a strong correlation between cTnI values and infarct mass at 24 (n = 24), 48 (n = 26), 72 (n = 23), and 96 h (n = 28) after onset of symptoms (Fig. 1A
and B). As with other studies (2)(3), correlations between the infarct size and cTnI were significant for all time-points except for admission (Spearman correlation coefficient Rho = 0.2; data not shown).
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These data document that cTnI values provide accurate estimates of infarct size in patients with STEMI. As with cTnT (2)(3), cTnI correlated with infarct size in reperfused STEMI patients at 24–96 h as well (Fig. 1A
). These data indicate that clinicians can rely on values on days 1–4 to provide an approximation to MRI-determined reperfused infarct size. Importantly, the slopes of the correlation curves are different for each day (Fig. 1B
). The parallelism of these data with the data for cTnT suggest that similar relationships, as with cTnT, are also likely to occur with non-STEMI. It is also likely that there will be differences with and without reperfusion. The use of imaging techniques such as positron-emission tomography and contrast-enhanced MRI (4) to enable determination of infarct size are currently impeded owing to limited availability and high cost. Small infarcts may escape visualization because of inadequate resolution. We now show with MRI that single-point values of cTnI between 24 and 96h, as with sestamibi measurements (5), correlate well. Troponin measurements are not only cheaper and more available but provide an estimate of the size of infarction not confounded by prior infarction. This investigation shows that for patients with reperfused STEMI, early as well as later measurements of cTnI are reliable estimates of infarct size. The fact that cTnI measurement at time-points earlier than 96 h correlate well with MRI-determined infarct size should allow for an earlier evaluation of prognosis in of these patients. Larger prospective and controlled studies are needed to confirm our results.
Acknowledgments
Grant/funding Support: None declared.
Financial Disclosures: E.G. has received financial support for studies from Roche Diagnostics and is consultant to Roche. H.A.K. developed the assay for cTnT and holds a patent jointly with Roche Diagnostics. He has received research support from Roche Diagnostics. A.S.J. is a consultant and has received research support from Dade-Behring and Beckman-Coulter. He is a consultant to Ortho Diagnostics and has consulted over time for most of the major diagnostic companies.
References
The following articles in journals at HighWire Press have cited this article:
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  A. S. Jaffe Key Issues in the Developing Synergism between Cardiovascular Imaging and Biomarkers Clin. Chem., September 1, 2008; 54(9): 1432 - 1442. [Abstract] [Full Text] [PDF]
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