Growth patterns and cerebroplacental hemodynamics in fetuses with congenital heart disease

Mebius, Mirthe J; Clur, S. A.; Vink, Arja S.; Pajkrt, Eva; Kalteren, Willemien S; Kooi, Elisabeth M. W.; Bos, Arie; Sarvaas, Gideon J. du Marchie; Bilardo, C. M.

doi:10.1002/uog.19102

Cited by 22 publications

(33 citation statements)

References 35 publications

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“…This is in contrast to another study of pregnancies complicated by fetal CHD, serial measures of fetal biometry and cerebroplacental Doppler flow were measured in the second half of pregnancy showed normal Doppler flow patterns, and did not find any significant relationship between placental function (as measured by Doppler studies of the UA and CPR) and fetal head growth (36). More specifically, even though MCA Doppler values varied between sub-groups of CHD, there was no association between MCA Doppler values and head growth in this population of CHD (36). Differences between studies may reflect differences in sample size (44 vs. 181, respectively), but again, also differences in CHD sub-types and sub-group classification.…”

contrasting

confidence: 99%

Placental abnormalities in congenital heart disease

Andescavage¹,

Limperopoulos²

2021

Transl Pediatr

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Congenital heart disease (CHD) remains the most common birth defect in infants, and critical CHD is associated with significant rates of morbidity and mortality. With the advent of powerful yet noninvasive advanced fetal imaging, it is becoming increasingly evident that the presence of CHD in utero disrupts typical development and contributes to the lifelong morbidity in this population. Across healthy and high-risk populations, intrauterine influences can permanently alter fetal development that may manifest in complex morbidities later in life, the so-called fetal-onset-of-adult-disease (FOAD) phenomenon. The placenta plays a critical role in not only supporting fetal development, but also by adapting to specific intrauterine conditions. The role of placental health, adaptation and dysfunction, however, in CHD is not well understood. In this article, we will review current evidence relating placental health in CHD, appraise existing knowledge-gaps in the field and highlight promising new avenues to better understand the impact of placental function on fetal well-being. We will review evidence of ex vivo human placental studies that describe abnormal placental findings in pregnancies complicated by CHD, as well evidence for in vivo assessments of the human placenta. While overall clinical in vivo assessments of placental development are rather limited, we will also review emerging evidence from advanced quantitative and functional magnetic resonance imaging that are bringing new insights into placental structure and function throughout gestation.By providing novel information about placental development, we can now explore the maternal-fetalplacental connection in greater detail, and better understand the multi-factorial mechanisms that may contribute to adverse outcomes seen in survivors of CHD.

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contrasting

confidence: 99%

Placental abnormalities in congenital heart disease

Andescavage¹,

Limperopoulos²

2021

Transl Pediatr

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“…However, our recent, large cohort study, which made several antenatal HC measurements in cases with isolated CHD, could not replicate these results, finding only small differences in fetal head growth, with HC values that remained within the normal range, irrespective of alterations in aortic flow or saturation. Two more recent, large cohort studies also opposed the hypothesis of decreased oxygenation as an explanation for smaller HC, and showed very small differences in HC between normal and CHD fetuses. A noteable finding was that small changes in HC size were also encountered in cases with a type of CHD that does not result in fetal circulatory changes.…”

Section: Introductionmentioning

confidence: 76%

“…To study brain development in utero , several cohort studies have reported on head circumference (HC) as a proxy for neurocognitive outcome, as fetal head size is related directly to brain volume. These studies reported a lower mean HC in fetuses and neonates with CHD, particularly in those with hypoplastic left heart syndrome and transposition of the great arteries, compared to the average in the general population.…”

Section: Introductionmentioning

confidence: 99%

Impact of extracardiac pathology on head growth in fetuses with congenital heart defect

Nisselrooij

Jansen

Geloven

et al. 2019

Ultrasound in Obstet & Gyne

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Objective Neurodevelopmental delay is frequently encountered in children with a congenital heart defect (CHD). Fetuses with major CHD have a smaller head circumference (HC), irrespective of altered cerebral flow or brain oxygenation. This cohort study compared head growth in cases with isolated vs those with non‐isolated CHD to evaluate the effect of additional pathology on head size in these fetuses. Method All CHD cases diagnosed prenatally in the period January 2002–July 2014 were selected from our regional registry, PRECOR. Cases of multiple pregnancy, and those affected by maternal diabetes, severe fetal structural brain anomalies or functional CHD were excluded. Subjects were divided into groups according to whether the CHD was isolated, and the non‐isolated group was subdivided into three groups: cases with genetic anomaly, extracardiac malformation or placental pathology. In both isolated and non‐isolated CHD groups, CHDs were also grouped according to their potential effect on aortic flow and oxygen saturation. Mean HC Z‐scores at 20 weeks and increase or decrease (Δ) of HC Z‐scores over the course of pregnancy were compared between isolated and non‐isolated groups, using mixed linear regression models. Results Included were 916 cases of CHD diagnosed prenatally, of which 378 (41.3%) were non‐isolated (37 with placental pathology, 217 with genetic anomaly and 124 with extracardiac malformation). At 20 weeks, non‐isolated cases had significantly lower HC Z‐scores than did isolated cases (Z‐score = –0.70 vs –0.03; P < 0.001) and head growth over the course of pregnancy showed a larger decrease in this group (Δ HC Z‐score = –0.03 vs –0.01 per week; P = 0.01). Cases with placental pathology had the lowest HC Z‐score at 20 weeks (Z‐score = –1.29) and the largest decrease in head growth (Δ HC Z‐score = –0.06 per week). In CHD subjects with a genetic diagnosis (Z‐score = –0.73; Δ HC Z‐score = –0.04 per week) and in those with an extracardiac malformation (Z‐score = –0.49; Δ HC Z‐score = –0.02 per week), HC Z‐scores were also lower compared with those in subjects with isolated CHD. CHDs that result in low oxygenation or flow to the brain were present more frequently in isolated than in non‐isolated cases. Conclusions Smaller HC in fetuses with CHD appears to be associated strongly with additional pathology. Placental pathology and genetic anomaly in particular seem to be important contributors to restricted head growth. This effect appears to be irrespective of altered hemodynamics caused by the CHD. Previously reported smaller HC in CHD should, in our opinion, be attributed to additional pathology. Neurodevelopment studies in infants with CHD should, therefore, always differentiate between isolated and non‐isolated cases. © 2019 The Authors. Ultrasound in Obstetrics & Gynecology published by John Wiley & Sons Ltd on behalf of the International Society of Ultrasound in Obstetrics and Gynecology.

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“…Umbilical artery Doppler waveforms and pulsatility index (PI) are routinely assessed in obstetrical ultrasound and fetal echocardiography, but fall in the normal range for fetuses with CHD. 8 Given the recently demonstrated high prevalence of postnatal placental pathologic findings in CHD fetuses, 7 umbilical arterial Doppler waveforms may be insufficiently sensitive to reflect these differences. In the setting of increased downstream placental vascular resistance, a decrease in blood flow could falsely normalize a pulsatility index.…”

Section: Introductionmentioning

confidence: 99%

“…The placenta normally acts as a low resistance sink to which the fetal heart sends blood via the umbilical arteries, allowing for gas and nutrient transfer prior to returning to the fetal circulation via the umbilical vein. Umbilical artery Doppler waveforms and pulsatility index (PI) are routinely assessed in obstetrical ultrasound and fetal echocardiography, but fall in the normal range for fetuses with CHD 8 . Given the recently demonstrated high prevalence of postnatal placental pathologic findings in CHD fetuses, 7 umbilical arterial Doppler waveforms may be insufficiently sensitive to reflect these differences.…”

Section: Introductionmentioning

confidence: 99%

Mid‐gestational fetal placental blood flow is diminished in the fetus with congenital heart disease

Josowitz

Katcoff

et al. 2020

Prenatal Diagnosis

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Objective: Data suggest fetuses with congenital heart disease (CHD) have placental abnormalities. Their abnormal placental vasculature may affect fetal placental blood flow, which has not previously been explored. Method: We performed a retrospective cross-sectional study comparing umbilical venous volume flow (UVVF) of single ventricle, D-transposition of the great arteries, and tetralogy of Fallot fetuses with fetuses without CHD. UVVF and combined cardiac output (CCO) were calculated from fetal echocardiography and compared using t tests, χ 2 and Fisher's exact tests. Results: Mean gestational age and fetal weight were greater in CHD fetuses (26.5 weeks, 1119.4 g; n = 81, P < .001) compared to controls (23.1 weeks, 675 g; n = 170, P < .001). UVVF/fetal weight was nevertheless decreased among cases (99.8 vs 115.3 mL/min/kg, P < .001). Subgroup analysis of 20-to 25-week fetuses demonstrated no significant differences in case and control baseline characteristics. In CHD fetuses (n = 31) compared to controls (n = 144), absolute UVVF (50.8 vs 62.1 mL/min, P = .006), and UVVF/fetal weight (98.8 vs 118.5 mL/min/kg, P < .001) were decreased. Findings were similar in single ventricle (n = 24) and hypoplastic left heart syndrome (n = 14). Conclusion: Mid-gestational placental blood flow in CHD fetuses is decreased compared to controls. Further study is needed to explore the relationship between UVVF and placental pathology, and impact on outcomes.

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Growth patterns and cerebroplacental hemodynamics in fetuses with congenital heart disease

Cited by 22 publications

References 35 publications

Placental abnormalities in congenital heart disease

Placental abnormalities in congenital heart disease

Impact of extracardiac pathology on head growth in fetuses with congenital heart defect

Mid‐gestational fetal placental blood flow is diminished in the fetus with congenital heart disease

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