Why the study?
Does in utero exposure to beta-sympathomimetic tocolytic therapy increase cardiac troponin T levels in cord blood of neonates?
Does in utero exposure to beta-sympathomimetic tocolytic therapy increase cardiac troponin T levels in cord blood of neonates?
Acute tocolytic therapy with beta-sympathomimetics increases cord blood cTnT levels, suggesting cTnT is a more useful marker for neonatal myocardial injury than CK-MB in this setting.
Should not yet change tocolysis practice; leaves open whether elevated cTnT signals clinically relevant myocardial injury.
The present study was designed to determine the levels of cardiac troponin T (cTnT) in cord blood of neonates exposed in utero to tocolytic therapy by beta-sympathomimetics. cTnT in 40 neonates after acute tocolysis (0.24 +/- 0.05 microg/l) was significantly higher (p < 0.05) in comparison with the control group (0.05 +/- 0.01 microg/l). The maximal values were reached in about the 3rd day of therapy (0.39 +/- 0.11 microg/l). cTnT in 30 neonates after long-term tocolysis was 0.12 +/- 0.03 microg/l. No correlation was found between cTnT and CK and its isoenzyme CK-MB or ECG. CK, unlike cTnT, significantly correlated with gestational age (r = 0.57, p < 0.05) and birth weight (r = 0.55, p < 0.05). It is possible to conclude that acute tocolytic therapy by beta-sympathomimetics increases the cTnT levels in cord blood and cardiac troponin T is more useful for the laboratory diagnosis of neonatal myocardial injury than CK-MB.
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Adamcová et al. (2000) studied this question.
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