Troponin I as a Biomarker of Cardiac Injury in Neonates with Idiopathic Respiratory Distress

Abstract

Troponin I (TnI), an inhibitory protein complex located on the actin filament of cardiac muscle, has become a specific marker of myocardial damage. Troponin has been studied in a wide range of clinical settings. However, many questions are still unanswered, especially in preterm neonates with the most common pathology at birth, such as idiopathic respiratory distress syndrome (IRDS). The aim of this study was to establish a reference range for cardiac TnI for healthy preterm infants and serum levels in sick preterm infants with IRDS. Echocardiography was performed and TnI serum levels were measured at a median age of 62 hours of life in three groups of healthy preterm infants (n = 10), and ventilated infants with moderate (n = 15) and severe IRDS (n = 15). Ventilated infants with idiopathic moderate IRDS had significantly different cardiac parameters (R/L ejection fraction, R/L stroke volume, R/L cardiac output; p < 0.05) and significantly higher cardiac TnI levels than healthy infants (0.037 versus 0.01 microg/mL; p < 0.05). Furthermore, infants with severe IRDS had higher TnI concentrations than infants with moderate IRDS (0.26 versus 0.037 microg/mL; p < 0.05). The results of this study show that increased TnI serum levels in sick preterm infants with IRDS are explained by myocardial injury or dysfunction due to impaired arterial oxygenation or reduction in cardiac output during treatment with mechanical ventilation. These results suggest that cardiac TnI may be a useful, specific marker for myocardial damage in preterm neonates with IRDS.

Perinatal Changes of Cardiac Troponin-I in Normal and Intrauterine Growth-Restricted Pregnancies

“…In addition, cTnI has been reported to be significantly elevated in the cord blood of critically ill newborns and even higher in nonsurvivors [20], implying that cTnI could serve as a predictor of mortality in this group of newborns. Furthermore, increased levels of cTnI were associated with a lower umbilical artery pH [21], and have been reported in sick preterm neonates with idiopathic respiratory distress [22]. …”

Actualities on molecular pathogenesis and repairing processes of cerebral damage in perinatal hypoxic-ischemic encephalopathy

“…In this way, rising pressure increases CBF and can cause haemorrhagic phenomena, while low pressure reduces CBF and can cause ischemic phenomena. It has to be kept in mind that systemic arterial hypotension is frequent in high-degree premature infants who present cardiac contractile function and sympathetic vascular tone immaturity, and in all newborns with perinatal asphyxia, resulting from impaired myocardial contractility induced by hypoxia and acidosis [5]. This explains why these infants are particularly exposed to cerebral ischemia.…”

Serum Troponin in Neonatal Intensive Care

“…The NE and perinatal hypoxia group without NE had a significantly higher cord blood cTnI compared to controls (1. [40] measured cTnI levels in preterm infants at a mean of 62 h. 10 infants had no RDS, 15 had moderate and 15 had severe RDS, and all were matched for gestation and birth weight. cTnT levels were highest in the severe group (0.26 8 0.04 g/l) followed by the moderate group (0.037 8 0.01 g/l) and controls (0.1 8 0.01 g/l).…”