Abstract
Glucocorticoids are essential in mammals to mature fetal organs and tissues in order to survive after birth. Hence, antenatal glucocorticoid treatment (termed antenatal corticosteroid therapy) can be life-saving in preterm babies and is commonly used in women at risk of preterm birth. While the effects of glucocorticoids on lung maturation have been well described, the effects on the fetal heart remain less clear. Experiments in mice have shown that endogenous glucocorticoid action is required to mature the fetal heart. However, whether the potent synthetic glucocorticoids used in antenatal corticosteroid therapy have similar maturational effects on the fetal heart is less clear. Moreover, antenatal corticosteroid therapy may increase the risk of cardiovascular disease in adulthood. Here, we present a narrative review of the evidence relating to the effects of antenatal glucocorticoid action on the fetal heart and discuss the implications for antenatal corticosteroid therapy.
Highlights
Through most of gestation, the mammalian fetus is maintained in a low glucocorticoid environment, with fetal glucocorticoid concentrations typically five- to tenfold lower than maternal
The reduced heart mass after preterm birth becomes normalised by disproportionate cardiac hypertrophy and increased left ventricular mass in subsequent ‘catch-up’ growth in the early postnatal period (Kozak-Barany et al 2001, Aye et al 2017), with differences in cardiac structure and function persisting in adulthood
Preterm birth is strongly associated with increased risk of cardiovascular disease in later life, the evidence to date suggests that effects of preterm birth on cardiac morphology and function are independent of antenatal corticosteroid exposure (Dalziel et al 2005, Aye et al 2017)
Summary
The mammalian fetus is maintained in a low glucocorticoid environment, with fetal glucocorticoid concentrations typically five- to tenfold lower than maternal. Expression profiling and in silico transcription factor analysis in sheep heart across the perinatal period suggests glucocorticoids transiently suppress immune responses at birth and that they support metabolic changes during the transition from fetal to neonatal life (Richards et al 2015).
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