J. Mair et al., CARDIAC TROPONIN-I RELEASE CORRELATES WITH MYOCARDIAL-INFARCTION SIZE, European journal of clinical chemistry and clinical biochemistry, 33(11), 1995, pp. 869-872
Cardiac troponin I, creatine kinase, and creatine kinase MB activity w
ere tested in serial blood samples from 15 patients with first-lime Q
wave acute myocardial infarction (2 anterior and 13 inferior wall infa
rctions). All patients received intravenous thrombolytic therapy. Card
iac troponin I and creatine kinase MB activity were compared with scin
tigraphic estimates of myocardial scar (single photon emission compute
d tomography [SPECT] with (99m)Technetium-isonitrile [Tc-sestamibi]) o
n late images at rest about 5 weeks after myocardial infarction. Scint
igraphic defect sizes ranged from 3.2 to 41.2% (median: 27.3%) of left
ventricle. Cardiac troponin I increased and peaked in parallel with c
reatine kinase MB activity, and the peak values correlated with each o
ther (r = 0.76, p = 0.002). Troponin I stayed increased for several da
ys longer than creatine kinase and creatine kinase MB activity. It cou
ld be detected at least until the 4th day after admission. Significant
correlation coefficients were found between Tc-99m-isonitrile defect
sizes and areas under cardiac troponin I curves (r = 0.53, p = 0.042)
and between Tc-99m-isonitrile defect sizes and cumulative creatine kin
ase MB activity release (r = 0.64, p = 0.01). Animal studies have alre
ady shown a very close correlation between histologic infarct size and
SPECT Tc-99m-isonitrile defect size. Therefore, our results indicate
that cardiac troponin I release in patients with infarct size.