Impaired placental perfusion and major fetal cardiac defects

Abstract

Objective To investigate the relationship between fetal congenital heart defects (CHD) and placental perfusion assessed by uterine artery pulsatility index (UtA‐PI), in relation to development of pre‐eclampsia (PE). Methods This was a prospective screening study of singleton pregnancies at 19–24 weeks' gestation. Transvaginal ultrasound was used to measure UtA‐PI and the values were converted into multiples of the normal median (MoM). Median MoM values in pregnancies with a fetus with isolated major CHD were compared to those without CHD, in relation to development of PE. Results The 91 407 singleton pregnancies fulfilling the entry criteria included 206 (0.23%) with isolated major fetal CHD and 91 201 without CHD. The prevalence of PE was 4.4% in pregnancies with fetal CHD and 2.7% in those without CHD (relative risk (RR), 1.6 (95% CI, 0.84–3.04); P = 0.150); the respective values for preterm PE with delivery at < 37 weeks' gestation were 2.4% and 0.7% (RR, 3.4 (95% CI, 1.42–8.09); P = 0.006). In the total population, median UtA‐PI MoM was significantly higher in those that developed PE compared to those without PE (1.22 (interquartile range (IQR), 0.94–1.57) vs 1.00 (IQR, 0.84–1.19); P < 0.0001) and, in the PE group, the median UtA‐PI MoM was inversely related to gestational age at delivery (r = −0.458; P < 0.0001). The same pattern of inverse relationship between UtA‐PI MoM and gestational age at delivery with PE was observed in pregnancies with and those without CHD, but, in the CHD group, compared to those without CHD, UtA‐PI was significantly higher both in pregnancies with and in those without PE. Conclusions In pregnancies both with and without fetal CHD that develop PE, impedance to flow in the UtAs is increased and this increase is particularly marked in those with preterm PE. The prevalence of preterm PE is more than three times higher in pregnancies with than those without fetal major CHD, and the prevalence of major CHD in pregnancies with preterm PE is also more than three times higher than in those without PE. However, > 97% of pregnancies with fetal CHD do not develop preterm PE and > 99% of pregnancies with preterm PE are not associated with fetal CHD. Copyright © 2018 ISUOG. Published by John Wiley & Sons Ltd.

Adverse perinatal outcome and placental abnormalities in pregnancies with major fetal congenital heart defects: A retrospective case‐control study

“…1 Such placental impairment might be associated with underperfusion resulting in an increase in the uterine artery pulsatility index (UtA-PI) in mid-pregnancy in CHD pregnancies. 2 Compared to those without CHD, median UtA-PI is significantly higher in the pregnancies with CHD, both in pregnancies with and in those without PE.…”

“…[3][4][5][6][7] Moreover, first-trimester markers of placental function such as PAPP-A and PlGF have been found to be lower in CHD pregnancies than in matched pregnancies with structurally normal hearts suggesting that in isolated CHD there is a placental dysfunction which is already established from the first trimester. 1,2,15,16 However, imbalances in placental angiogenic factors (sFLT and PlGF) have been found to be shown in pregnancies without known placental dysfunction reflecting perhaps the common origin of the heart and placenta. 15 Besides these placental morpho-functional aspects, previous studies have outlined that PE was more frequent in pregnancies affected by fetal CHD.…”

“…1 However, published studies report controversial data on the association between impaired placentation and CHD. 2 Histological examination of the placenta in the presence of CHD has demonstrated a broad range of anomalies, including reduced absolute placental weight, a lower placental weight-to-newborn birthweight ratio and a number of vascular abnormalities such as chorangiosis, villus maturity and thrombosis. [3][4][5] Abnormal placental cord insertion is more common in placentas from pregnancies with fetal CHD.…”

“…Preterm preeclampsia (PE) is three times more common in pregnancies with fetal major CHD, and the prevalence of major CHD in pregnancies with preterm PE is also more than three times higher than in those without CHD 1 . However, published studies report controversial data on the association between impaired placentation and CHD 2 . Histological examination of the placenta in the presence of CHD has demonstrated a broad range of anomalies, including reduced absolute placental weight, a lower placental weight‐to‐newborn birthweight ratio and a number of vascular abnormalities such as chorangiosis, villus maturity and thrombosis 3‐5 .…”

Placental DNA methylation changes in detection of tetralogy of Fallot

“…The placenta appears to play a critical role in the development of CHD. In a recent mid‐trimester study, uterine artery Doppler pulsatility index, an indirect measure of placental angiogenesis, demonstrated increased resistance in CHD pregnancies compared with controls, supporting the relationship between the placental vasculature and CHD development. The placenta could therefore be an ideal tissue for both understanding the mechanism of and providing biomarker development for CHD.…”