Abstract
AimsFetuses affected by congenital heart defects (CHD) are considered to be at increased risk of fetal growth restriction and intrauterine demise. Whether these risks are a direct consequence of fetal CHD or a result of associated uteroplacental dysfunction is not evident from the data of recent studies. The aim of this study was to investigate the prevalence of uteroplacental dysfunction reflected by abnormal uterine artery Doppler indices and reduced fetal growth in CHD pregnancies.MethodsThis is a retrospective case-control study including singleton pregnancies referred for detailed fetal cardiac assessment subsequently diagnosed with or without CHD. Mid-trimester uterine artery Doppler assessment at 20–24 weeks as well as third trimester fetal biometry and arterial Doppler pulsatility indices (PI) were performed. All fetal biometry were converted into centiles and Doppler values to multiples of median (MoM) to adjust for physiological changes with gestation.ResultsThe study included 811 pregnancies including 153 cases where the fetus was diagnosed with CHD. Mid-pregnancy uterine artery PI was significantly higher in women with fetal CHD compared to controls (0.90MoM vs 0.83MoM; p = 0.006). In the third trimester, median centiles for fetal head circumference (45.4 vs 57.07; p<0.001), abdominal circumference (51.17 vs 55.71; p = 0.014), estimated fetal weight (33.6 vs 56.7; p<0.001) and cerebroplacental ratio (CPR: 0.84MoM vs 0.95MoM; p<0.001) were significantly lower in fetuses with CHD compared to controls. The percentage of small for gestational age births <10th centile (24.0% vs 10.7%; <0.001) and low CPR <0.6MoM (11.7% vs 2.5%; p<0.001) were significantly higher in the fetal CHD cohort.ConclusionsMid-pregnancy uterine artery resistance is increased and subsequent fetal biometry reduced in pregnancies with CHD fetuses. These findings suggest that fetal CHD are associated with uteroplacental dysfunction, secondary to impaired maternal uteroplacental perfusion resulting in relative fetal hypoxaemia and reduced fetal growth.
Highlights
Congenital heart defects (CHD) affect around 1% of live births and are considered the leading cause of neonatal mortality due to birth defects [1]
Mid-pregnancy uterine artery pulsatility index (PI) was significantly higher in women with fetal CHD compared to controls (0.90MoM vs 0.83MoM; p = 0.006)
Median centiles for fetal head circumference (45.4 vs 57.07; p
Summary
Congenital heart defects (CHD) affect around 1% of live births and are considered the leading cause of neonatal mortality due to birth defects [1]. Recent data suggest uteroplacental malperfusion as an additional or even underlying mechanism in fetuses with CHD describing decreased levels of placental like growth factor (PLGF) in isolated major CHD in the first trimester, indicating impaired placentation [8, 9]. Soluble fms-like tyrosine kinase 1 (sFlt-1), vascular endothelial growth factor A and soluble endoglin, markers of antiangiogenesis, were expressed in higher amounts in fetal heart tissue and fetal cord blood when a CHD was present [10]. Maternal serum of women carrying a fetus with a CHD showed decreased PLGF and increased sFlt levels, which is hypothesized to be due to impaired placental angiogenesis [10]
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