Cardiac troponin I should be interpreted with caution in paediatric neonatal patients. Concerning Turker et al.: 'Cord blood cardiac troponin I as an early predictor of short-term outcome in perinatal hypoxia'.

Accessible online at: www.karger.com/bon There have been recent reports of using cardiac troponin I (cTnI) as a marker in myocardial damage in neonates [1, 2]. These reports have provided controversial data. During development, a foetal isoform of cardiac troponin T (cTnT) is transiently expressed in skeletal muscle [3], but is downregulated in adult skeletal muscle tissue [4]. In foetal cardiac tissue, 5 isoforms of cTnT are expressed; however, no skeletal TnT is expressed [5]. During the development of the foetus, the dominant form of troponin I appears as slow muscle skeletal TnI (sTnI), which is down-regulated with concurrent upregulation of cTnI expression during the first 9 months of life [6]. Therefore, cTnI is not a suitable candidate biomarker of cardiomyocyte damage in the neonatal period [7]. This concept has not been addressed by some authors [1, 2]; however, their data may either challenge this notion or may be attributable to an infiltration of maternal blood carrying cTnI into the placenta during parturition. It has been shown that circulating maternal cTnI is detectable in mothers who suffer myocardial ischaemia during postpartum haemorrhage [8], but levels of maternal cTnI are not affected by either vaginal or caesarean modes of delivery [9].