Abstract
Background: In spite of its potential clinical prognostic significance, only a small number of studies have been conducted to date involving neonatal cardiac troponin-I as an early indicator of significance respiratory dysfunction. Objective: Aim of this study was to evaluate the clinical significance cardiac troponin-I as marker of cardiorespiratory failure in term newborns. Methods: Cardiac troponin-I level was determined in serum (at 24-48 hours after birth) in 55 term neonates with respiratory distress and 36 healthy, term newborns. The cardiac troponin-I level is correlated with the total duration of oxygen and ventilatory therapy (expressed in days) in both groups with (13/55) or without (32/55) deaths. Results: Newborns with respiratory distress had a significantly higher level of cardiac troponin-I, compared to the control group, with the largest increase in cardiac troponin-I observed in mechanically ventilated patients (31/55). The length of applied respiratory support was positively correlated with the level of cardiac troponin-I in survivors of respondents, while in the group of children who died the level of cardiac troponin-I was negatively correlated with total duration of respiratory support, and the number of days to death. Conclusions: The increase in cardiac troponin-I could indicate the development of severe respiratory failure in term neonates with respiratory distress.
Highlights
Markers of myocardial damage are the macromolecules, which after myocardial necrosis diffuse to the cardiac intersticium and microvasculature
The increase in cardiac troponin-I could indicate the development of severe respiratory failure in term neonates with respiratory distress
The specificity of cardiac markers is reflected in high concentrations in the myocardium and absence in other tissues, while the sensitivity of these markers is reflected in speed of their release into the blood after myocardial damage [1]
Summary
Markers of myocardial damage are the macromolecules, which after myocardial necrosis diffuse to the cardiac intersticium and microvasculature. Markers of myocardial necrosis, which is commonly used in clinical practice are: creatine kinase and its isoenzyme creatine kinase-muscle, troponin I and T, lactate dehydrogenase, myoglobin, and others [2,3,4,5]. Troponin complex consists of three subunits that regulate the contractile process in muscle interfering calcium ions. The three subunits are: Troponin C (18 kD), which binds to calcium ions, Troponin I (26 kD) that binds to actin and inhibits the reaction between actin and myosin and Troponin T (39 kD), which binds to tropomyosin. In spite of its potential clinical prognostic significance, only a small number of studies have been conducted to date involving neonatal cardiac troponin-I as an early indicator of significance respiratory dysfunction
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