Introduction: Fetal Growth Restriction is a significant source of perinatal morbidity. Mothers with congenital heart disease (CHD) have a higher incidence of neonates who are small for gestational age (SGA) compared to the general population. It has been hypothesized that this results from altered maternal-feto-placental physiology. We asked whether Doppler markers of abnormal placental and cerebral resistance in fetuses of mothers with CHD predict subsequent low birth weight or asymmetric fetal growth.
Hypothesis: Doppler markers of cerebro-placental resistance will be associated with anthropometric outcomes.
Methods: The study population included 94 mothers with CHD who had 115 pregnancies, underwent mid-gestation fetal echocardiograms, and delivered a live-born infant. Mothers were classified according to WHO risk score in pregnancy. Umbilical Artery (UA) and Middle Cerebral Artery (MCA) pulsatility indices (PI) and Cerebroplacental Ratio (CPR) were measured retrospectively from stored images taken during routine fetal echocardiography. Logistic and linear regression were performed for dichotomous and continuous variables respectively.
Results: The prevalence of SGA was 5% higher than in the general population. Women with complex heart disease had higher rates of perinatal complications than those with simple disease (36% vs 24 %) and their babies had a lower birth percentile (coef. -11.3 P=0.021, CI -20.93,- 1.75). No association was found between UA PI, MCA PI, CPR and birth percentile. However, when dichotomizing the group as normal vs SGA and adjusting for gestational age at fetal echo, neonates who were SGA had a higher UA PI than those who were not SGA (P=0.05).
Conclusions: Women with CHD, particularly those with severe disease, have a high rate of fetal growth restriction and more perinatal complications. Although SGA infants had a higher UA PI in mid-gestation, there was no relationship between fetal Doppler patterns and birth percentile in the entire cohort. The mechanism of growth impairment in this population may be secondary to physiologic aberrations occurring later in gestation as maternal physiology is most altered in the third trimester. Further study is required looking at late gestation fetal echoes of mothers with CHD.