Myocardial Ischaemia in Aphyxia Neonatorum

Primhak, Robert; Jedeikin, Roy; Ellis, Graham; Makela, Sinikka K.; Gillan, John; Swyer, Paul R.; Rowe, Richard D.

doi:10.1111/j.1651-2227.1985.tb11036.x

Cited by 51 publications

(17 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Unlike the complete regional ischaemia that the adult heart gets, infants have a diffuse hypoxic ischaemia because of reduced oxygen delivery [10,22]. It is likely that this causes scattered myocyte loss in the heart and this would be supported by the diffuse myocardial injury seen in severe cases of perinatal asphyxia [10,19,25].…”

Section: Myocardial Performance and Cardiac Troponin Tmentioning

confidence: 97%

Sequential cardiac troponin T following delivery and its relationship with myocardial performance in neonates with respiratory distress syndrome

et al. 2005

View full text Add to dashboard Cite

We measured serial cardiac troponin T in babies with respiratory distress syndrome and in "healthy" controls (no cardiorespiratory support required). We investigated relationships between cardiac troponin T and myocardial performance in respiratory distress syndrome. This was a prospective observational study at a large tertiary maternity unit that recruited 104 "healthy" babies from whom individual samples were collected. A further 24 infants with respiratory distress syndrome and 14 "healthy" preterm infants had serial sampling over the first three days. We measured fractional shortening in 14 of the infants with respiratory distress syndrome. Cardiac troponin T rose from a median (interquartile range) of 10 (10-11) pg/mL on day one to 34 (22-46) pg/mL by day three, p=0.005, in "healthy" babies. In respiratory distress syndrome levels were higher, 91 (46-135) pg/mL at 6 (5-7) hours of age, p<0.001, and remained so for all three days. In babies with respiratory distress syndrome on day one cardiac troponin T correlated negatively with fractional shortening, Rho=-0.831, p<0.001, but this correlation did not persist. In "healthy" babies there is a minimal rise of cardiac troponin T by day 3. In respiratory distress syndrome there is an early and sustained elevation of cardiac troponin T, with a negative relationship with fraction shortening, suggesting significant myocardial damage of antenatal/intrapartum origin, giving rise to measurable dysfunction.

show abstract

Section: Myocardial Performance and Cardiac Troponin Tmentioning

confidence: 97%

Sequential cardiac troponin T following delivery and its relationship with myocardial performance in neonates with respiratory distress syndrome

et al. 2005

View full text Add to dashboard Cite

show abstract

“…Additionally, laboratory variables, indicating peripheral organ dysfunction, have been used extensively to retrospectively diagnose asphyxia [5,15] . In the past, creatinine kinase and its isoenzyme MB have been frequently employed as biochemical markers of myocardial injury [6] . However, these markers have been largely discarded because gestation, sex, modes of delivery, and birth weight all affect creatine kinase levels [7] .…”

Section: Discussionmentioning

confidence: 99%

Cardiac Troponin I in Asphyxiated Neonates

Trevisanuto¹,

Picco²,

Golin³

et al. 2006

Neonatology

View full text Add to dashboard Cite

Background: Cardiac troponins T (cTnT) and I (cTnI) are well-established markers in detecting myocardial ischemic damage in adults. Perinatal asphyxia is associated with cardiac dysfunction. Objectives: To evaluate serum concentrations of cTnI in asphyxiated neonates and to investigate whether cTnI is correlated with the traditional markers of asphyxia. Methods: Blood samples were collected from 13 asphyxiated neonates (umbilical artery pH <7.18 and either a 1-min Apgar score <4 or a 5-min Apgar score <7) and 39 controls. Data on gestation, birth weight, sex, Apgar scores, mode of delivery, umbilical pH, creatinine, serum activity of aspartate and alanine aminotransferase, and QTc interval were investigated. Results: Median (range) cTnI concentrations were significantly higher in asphyxiated neonates with respect to healthy infants: 0.36 µg/l (0.05–11) versus 0.04 µg/l (0.04–0.06); p < 0.01. In asphyxiated babies, no statistically significant correlations were found between concentrations of cTnI and the other markers of asphyxia. Conclusions: In asphyxiated neonates, cTnI concentrations are higher with respect to healthy infants, suggesting the presence of myocardial damage in this group of high-risk patients. cTnI does not correlate with the traditional markers of asphyxia.

show abstract

“…6 Previous studies in neonates have used creatine kinase isoforms as biochemical markers of myocardial injury. 7 However, these markers have been largely discarded because gestation, sex, mode of delivery, and birth weight all affect creatine kinase activity. 7 8 Troponin is an inhibitory protein complex forming part of the contractile apparatus of all striated muscle, including the heart.…”

mentioning

confidence: 99%

Concentrations of cardiac troponin T in neonates with and without respiratory distress

Clark¹,

Newland²,

Yoxall³

et al. 2004

Archives of Disease in Childhood - Fetal and Neonatal Edition

View full text Add to dashboard Cite

Aims: To establish a practical postnatal reference range for cardiac troponin T in neonates and to investigate concentrations in neonates with respiratory distress. Methods: Prospective investigation in a tertiary neonatal unit, recruiting infants with and without respiratory distress (sick and healthy infants respectively). Concentrations of cardiac troponin T were compared between sick and healthy infants, accounting for confounding variables. Results: A total of 162 neonates (113 healthy and 49 sick infants) had samples taken. The median (interquartile range) cardiac troponin T concentration in the healthy infants was 0.025 (0.01-0.062) ng/ ml, and the 95th centile was 0.153 ng/ml. There were no significant relations between cardiac troponin T and various variables. The median (interquartile range) cardiac troponin T concentration in the sick infants was 0.159 (0.075-0.308) ng/ml. This was significantly higher (p , 0.0001) than in the healthy infants. In a linear regression model, the use of inotropes and oxygen requirement were significant associations independent of other basic and clinical variables in explaining the variation in cardiac troponin T concentrations. Conclusions: Cardiac troponin T is detectable in the blood of many healthy neonates, but no relation with important basic and clinical variables was found. Sick infants have significantly higher concentrations than healthy infants. The variations in cardiac troponin T concentration were significantly associated with oxygen requirement or the use of inotropic support in a regression model. Cardiac troponin T may be a useful marker of neonatal and cardiorespiratory morbidity.

show abstract

Myocardial Ischaemia in Aphyxia Neonatorum

Cited by 51 publications

References 19 publications

Sequential cardiac troponin T following delivery and its relationship with myocardial performance in neonates with respiratory distress syndrome

Sequential cardiac troponin T following delivery and its relationship with myocardial performance in neonates with respiratory distress syndrome

Cardiac Troponin I in Asphyxiated Neonates

Concentrations of cardiac troponin T in neonates with and without respiratory distress

Contact Info

Product

Resources

About