Cardiac troponin I at birth is of fetal-neonatal origin.

OBJECTIVE

Neonates produce predominantly skeletal muscle troponin I (TnI) in the myocardium; however, in asphyxiated neonates, high levels of cardiac troponin I (cTnI) have been found. We hypothesised that in these circumstances cTnI could be from the mother or the result of a change in fetal/neonatal production in response to an insult. In this study, we aimed to compare cTnI concentrations in asphyxiated neonates with those of their respective mothers.

METHODS

In this prospective observational study, we enrolled all asphyxiated neonates transferred by the Veneto Region Neonatal Transport Service in the period 1 January 2006 to 31 March 2007. Asphyxia was defined as a pH < or =7.00 and/or a base deficit of > or =16 mmol per litre. Neonatal and maternal blood samples were obtained for cTnI determination.

RESULTS

We enrolled 19 asphyxiated neonates (median gestational age: 39 weeks, interquartile range 34-40; birth weight 3100 g, 1950-3340). Their cTnI concentrations were significantly higher in comparison with their mothers: 0.24 microg/l (0.13-0.50) vs 0.04 microg/l (0.04-0.04); p<0.01.

CONCLUSIONS

Increased cTnI concentrations detected in asphyxiated neonates are of neonatal origin and are not derived from the mother. In asphyxiated neonates, there may be predisposing factors that could cause earlier switching from skeletal TnI to cTnI in the myocardium.