BACKGROUND: In most perinatal-hypoxia survivors, myocardial dysfunction can be reversed with appropriate inotropic support and oxygenation. The main problem related to outcome is cerebral damage. OBJECTIVE: We tested the hypothesis that cardiac troponin I (cTnI), a known marker of myocardial injury, is also an early predictor of severity of cerebral damage and mortality in intrauterine hypoxia. METHODS: Venous and arterial cord blood samples were collected at delivery from 54 consecutive newborns with hypoxic-ischemic encephalopathy and from 50 consecutive healthy controls. Arterial blood gas analysis was performed and levels of cTnI, creatine kinase and creatine kinase-MB in venous cord blood were measured. The same serum parameters were also measured on the 3rd and 7th day of life. RESULTS: Infants with hypoxia had a significantly higher cord blood cTnI levels than controls (p < 0.0001). Cord blood and 3rd and 7th day serum cTnI values showed a significant increase with severity of HIE (p < 0.0001). In non-survivors cord blood cTnI levels were significantly higher than the survivors (5.9 ng/ml, range 2.1-12.8, and 1.6 ng/ml, range 0.4-5.8, respectively; p < 0.0001). Receiver-operator curve analysis revealed cord cTnI as the most sensitive factor for predicting early death (area under curve = 0.956; SE: 0.028; 95% CI: 0.9-1.01). Cord blood cTnI of 4.6 ng/ml was identified as the optimal cut-off level for predicting serious risk of early mortality. CONCLUSION: The results suggest that significant elevation of cord cTnI is an excellent early predictor of severity of hypoxic-ischemic encephalopathy and mortality in term infants. Copyright 2004 S. Karger AG, Basel
BACKGROUND: In most perinatal-hypoxia survivors, myocardial dysfunction can be reversed with appropriate inotropic support and oxygenation. The main problem related to outcome is cerebral damage. OBJECTIVE: We tested the hypothesis that cardiac troponin I (cTnI), a known marker of myocardial injury, is also an early predictor of severity of cerebral damage and mortality in intrauterine hypoxia. METHODS: Venous and arterial cord blood samples were collected at delivery from 54 consecutive newborns with hypoxic-ischemicencephalopathy and from 50 consecutive healthy controls. Arterial blood gas analysis was performed and levels of cTnI, creatine kinase and creatine kinase-MB in venous cord blood were measured. The same serum parameters were also measured on the 3rd and 7th day of life. RESULTS:Infants with hypoxia had a significantly higher cord blood cTnI levels than controls (p < 0.0001). Cord blood and 3rd and 7th day serum cTnI values showed a significant increase with severity of HIE (p < 0.0001). In non-survivors cord blood cTnI levels were significantly higher than the survivors (5.9 ng/ml, range 2.1-12.8, and 1.6 ng/ml, range 0.4-5.8, respectively; p < 0.0001). Receiver-operator curve analysis revealed cord cTnI as the most sensitive factor for predicting early death (area under curve = 0.956; SE: 0.028; 95% CI: 0.9-1.01). Cord blood cTnI of 4.6 ng/ml was identified as the optimal cut-off level for predicting serious risk of early mortality. CONCLUSION: The results suggest that significant elevation of cord cTnI is an excellent early predictor of severity of hypoxic-ischemicencephalopathy and mortality in term infants. Copyright 2004 S. Karger AG, Basel
Authors: M A Cruz; Y A Bremmer; B O Porter; S D Gullquist; K L Watterberg; H J Rozycki Journal: Pediatr Cardiol Date: 2006 Jul-Aug Impact factor: 1.655
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Authors: Philip T Levy; Cecile Tissot; Beate Horsberg Eriksen; Eirik Nestaas; Sheryle Rogerson; Patrick J McNamara; Afif El-Khuffash; Willem P de Boode Journal: Pediatr Res Date: 2018-07 Impact factor: 3.756