Abstract
Intrauterine growth restriction (IUGR) implies fetal hypoxia, resulting in blood flow redistribution and sparing of vital organs (brain, heart). Serum cardiac Troponin-I (cTnI), a well-established marker of myocardial ischaemia, was measured in 40 mothers prior to delivery, the doubly clamped umbilical cords (representing fetal state), and their 20 IUGR and 20 appropriate-forgestational-age (AGA) neonates on day 1 and 4 postpartum. At all time points, no differences in cTnI levels were observed between the AGA and IUGR groups. Strong positive correlations were documented between maternal and fetal/neonatal values (r ≥ .498, P ≤ .025 in all cases in the AGA and r ≥ .615, P ≤ .009 in all cases in the IUGR group). These results may indicate (a) normal heart function, due to heart sparing, in the IUGR group (b) potential crossing of the placental barrier by cTnI in both groups.
Highlights
Cardiac troponin, an inhibitory protein complex located on the actin filament in all striated muscles, consists of three subunits T, I, and C [1] and coordinates striated muscle contraction in response to voltage changes [2]. cardiac Troponin-I (cTnI) is encoded by specific genes [3], blocks the formation of actinmyosin bridges [4] and since it is not found in skeletal muscles [5, 6], it is considered a highly specific indicator of myocardial injury in adults [4]
In the appropriate-forgestational age (AGA) group, no statistically significant differences in cTnI levels were observed between MS, umbilical cord (UC), N1, and N4
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
Summary
Cardiac troponin (cTn), an inhibitory protein complex located on the actin filament in all striated muscles, consists of three subunits T, I, and C [1] and coordinates striated muscle contraction in response to voltage changes [2]. cTnI is encoded by specific genes [3], blocks the formation of actinmyosin bridges [4] and since it is not found in skeletal muscles [5, 6], it is considered a highly specific indicator of myocardial injury in adults [4]. Intrauterine growth restriction (IUGR) caused by the chronic malnutrition and hypoxia [8, 9] (consequent to deficient placental transport of nutrients and oxygen [10], asymmetrical pattern of IUGR) is characterized by blood flow redistribution to vital organs (brain, myocardium, and adrenal glands), while other organs are deprived from sufficient blood flow. This phenomenon called “the brain-sparing effect” is usually accompanied by oligohydramnios [11, 12]. We aimed to determine circulating cTnI levels in IUGR and AGA pregnancies at time-points characteristic for intra-and extrauterine life, and correlate determined levels with gestational age, gender, and mode of delivery
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