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.