Data obtained in the present study show that scintigraphic versus serological estimation of infarct size is significantly correlated for each serum marker tested, independent of coronary reperfusion. The highest correlation coefficients were achieved with serum concentrations of TnT determined 72 hours after the onset of chest pain and with its cumulative concentrations. The correlation coefficients for the cumulative concentrations of CK and the other cytosolic enzymes were slightly better than for cumulative CK and cumulative TnT. This may be explained by the different release kinetics of the cytosolic enzymes and the properties of TnT as a structural protein. Estimation of infarct size, however, is more precise with cumulative TnT concentrations than with cumulative cytosolic enzyme concentrations, according to the correlation coefficient between scintigraphic estimation of infarct size and cumulative concentrations of marker proteins (table 4).
As serological markers for the estimation of infarct size, serum concentrations of CK, CK-MB, and LDH are mostly used. The accuracy of this approach, however, is adversely affected by several factors: The normal range of serum enzyme activity ranges from 10–80 IU/l for CK, < 10 IU/l for CK-MB, and 140–290 IU/l for LDH. Compared with this normal variation, the serum concentration increase of these cytosolic enzymes after AMI is relatively low. For example, CK and LDH activities increase < 60-fold and < 10-fold, respectively.19–21
Another disadvantage of cytosolic enzymes is their short persistence in the serum after AMI. CK and LDH serum concentrations decrease to normal concentrations within 3–6 days and 6–15 days, respectively.22–25
Furthermore, these cytosolic enzymes are also present in non-cardiac muscular tissues and can therefore be increased for other reasons, independent of myocardial cell damage, such as renal failure, myopathies, trauma, or even after vigorous exercise or in chronic alcoholism.7,8,26
In contrast to cytosolic enzymes, the baseline concentration of TnT is below the detection limit of commercially available assays but may exceed 400 times the discriminating serum concentration in myocardial cell damage.27
Compared with the cytosolic markers, TnT serum concentrations increase slightly earlier after the onset of symptoms at about 3.5 hours versus 4–8 hours (CK) and 6–12 hours (LDH).21
Since cross reactivity with skeletal TnT is < 1%, the specificity and sensitivity of TnT are about 96% and 100%, respectively.14
Because of the release kinetics of cytosolic enzymes, which reach a single, brief maximal peak within the first 24–48 hours after AMI and decrease to normal concentrations rapidly thereafter, serial blood sampling is mandatory to obtain the maximal or cumulative serum concentrations for estimation of infarct size. Prolonged TnT release over several days with a second peak on the third to fourth day allows a more precise estimation of infarct size over a longer period of time, even with a delay of several days after the onset of symptoms. When comparing the study groups in terms of peak serum CK concentration and infarct size estimated by scintigraphy (fig 4B, fig 5B), the gradient of the curve was greater in the reperfusion group than in the non-reperfusion group, reflecting a superincrease of maximal CK in the case of coronary reperfusion. In contrast with CK, the curve of TnT 72 hours after the onset of chest pain is not steeper in the reperfusion subgroup than in the non-reperfusion group (fig 4A, 5A); therefore, TnT 72 hours after the onset of chest pain seems to be almost unaffected by coronary reperfusion. The present study shows that a single blood sample 72 hours after the onset of symptoms allows a rather precise estimation of infarct size with serum TnT when compared with scintigraphic estimation. This result is supported by the findings of Kragten and colleagues.28
In 22 patients with AMI, these authors also showed that the cumulative as well as the second TnT peak concentration correlated significantly with the cumulative release of cytoplasmic enzyme in reperfused myocardial infarctions; however, their results were not related to infarct size.28
In addition to the methodological considerations mentioned above, further limitations have to be taken into account. Using thallium-201 SPECT imaging, assessment of infarct size can be improved by correcting for variable left ventricular mass in the individual segments. Also, the differing absorption in anterior and posterior myocardial segments was not corrected.
According to the present results, a single measurement of circulating TnT 72 hours after the onset of symptoms is a simple and reliable tool for serological estimation of myocardial infarct size independent of early coronary reperfusion.