Introduction
Over the last 40 years, the administration of antenatal corticosteroids
(ACS) has become routine practice in mothers with threatened preterm
labour between 24 and 34 weeks of gestation1. In this
circumstance, they are proven to reduce short-term neonatal morbidity -
especially that caused by respiratory distress syndrome,
intraventricular haemorrhage, necrotising enterocolitis and sepsis - and
mortality2 3. Prophylactic treatment
with ACS is designed to mimic the maturational effects of the normal
endogenous, prepartum increase in fetal plasma cortisol concentration
that occurs close to term in humans and other
species4. Glucocorticoids are known to switch tissue
accretion to differentiation. Therefore, ACS accelerate maturation of
many fetal organs and systems, enhancing the preterm baby’s successful
transition to neonatal life4 5.
Despite clear life-saving benefits of ACS, there is increasing awareness
of possible adverse off-target effects56 7. A systematic review in humans
showed improved major neurodevelopmental outcomes (e.g. lower rates of
cerebral palsy) in children exposed to ACS8, but a
large amount of animal data have suggested an association between ACS
administration and a range of neuro-anatomical and neuro-behavioural
changes 7 9 10.
The developing cardiovascular system is also affected by glucocorticoid
signalling. Preclinical animal studies have suggested that ACS may have
long-term adverse effects on the heart and the
circulation5 6 711 but much less is known about cardiovascular
consequences of ACS exposure in humans. Therefore, the aim of this study
was to systematically review the human clinical literature to determine
the effects of ACS on offspring cardiovascular function.