Cardiac troponin I at birth is of fetal-neonatal origin

Daniele Trevisanuto ^1*, Nicoletta Doglioni ¹, Sara Altinier ², Martina Zaninotto ², Mario Plebani ² and Vincenzo Zanardo ¹

¹ Pediatric Department, Medical School, University of Padova, Azienda Ospedaliera Padova, Italy
² Laboratory Medicine, Medical School, University of Padova, Azienda Ospedaliera Padova, Italy

^* To whom correspondence should be addressed. E-mail: trevo{at}pediatria.unipd.it.

Accepted 18 February 2009

Abstract

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 hypothesized that in these circumstances cTnI could be from the mother or a change in fetal/neonatal production in response to an insult. In this study, we aimed to compare cTnI concentrations in asphyxiated neonates and in 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 Jan 2006-31 Mar 2007. Asphyxia was defined as a pH<7.00 and/or a base deficit of >-16. Neonatal and maternal blood samples were obtained for cTnI determination (RxLHM, Dade Behringer).

Results: We enrolled 19 asphyxiated neonates (median gestational age: 39 wks, interquartile range 34-40; birth weight 3100 g, 1950-3340). Their cTnI concentrations were significantly higher in comparison with the mothers: 0.24 microg/L (0.13-0.50) vs 0.04 microgr/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.