Cardiac troponin I concentrations in neonates with hypoxic-ischaemic encephalopathy

Myocardial dysfunction is a frequent sequel of perinatal asphyxia. Cardiac troponin I (cTnI) is a marker of myocardial injury and a surrogate marker of myocardial dysfunction in adults, but there are few data in neonates. Our aim was to compare serum cTnI concentrations with clinical severity of encephalopathy and with duration of inotropic support in asphyxiated neonates.

Retrospective study of 60 neonates admitted with hypoxic-ischaemic encephalopathy (HIE). cTnI concentrations measured within 36 h of birth were compared with clinical grade of HIE (Sarnat-Sarnat classification) and with duration of inotropic support.

Serum cTnI concentrations and duration of inotropic support were significantly greater with increasing severity of HIE. Median (95% CI) cTnI concentrations were 0.04 μg/L (0.02-0.07 μg/L) in grade 1 HIE, 0.12 μg/L (0.08-0.20 μg/L) in grade 2 HIE and 0.67 μg/L (0.41-1.35 μg/L) in grade 3 HIE. Median (95% CI) duration of inotropic support required was 0 h (0-24 h) in grade 1 HIE, 28 h (0-118 h) in grade 2 HIE and 48 h (0-140 h) in grade 3 HIE.

In asphyxiated neonates, cTnI concentrations within 36 h of birth correlate strongly with clinical grade of HIE and with duration of inotropic support. Early cTnI concentrations may provide a useful proxy marker for the anticipated severity of myocardial dysfunction.