Characterization of the Placenta in the Newborn with Congenital Heart Disease: Distinctions Based on Type of Cardiac Malformation

Rychik, Jack; Goff, Donna A.; McKay, E.; Mott, Antonio R.; Tian, Zhenjun; Licht, Daniel J.; Gaynor, J. William

doi:10.1007/s00246-018-1876-x

Cited by 101 publications

(98 citation statements)

References 31 publications

(38 reference statements)

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“…Recent studies support that both growth restriction (17–18%) and placenta‐related complications, such as pre‐eclampsia, occur more frequently in CHD cases. However, as previous studies reporting on HC in CHD did not look at birth weight, growth trajectories or additional genetic pathology, their findings may, in our opinion, be explained by additional pathology.…”

Section: Discussionmentioning

confidence: 72%

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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Section: Discussionmentioning

confidence: 72%

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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“…Recent studies even reported morphological changes in brain structures in CHD fetuses using fetal MRI or three-dimensional ultrasound, which was correlated with severity of CHD [8,26,27]. Furthermore, a link between placental abnormalities and type of CHD has been reported by Rychik et al, who characterized the placenta in CHD and looked for distinctions based on type of malformation [28]. They found a high percentage of placental abnormalities in CHD newborns, including chorangiosis (18 %), hypomature villi (15 %), thrombosis (41 %) and infarction (17 %).…”

Section: Discussionmentioning

confidence: 99%

Head Biometry in Fetuses with Isolated Congenital Heart Disease

et al. 2018

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Purpose Altered cerebral hemodynamics are involved in changes in head biometry in fetuses with congenital heart disease (CHD). We compared head growth in different CHD groups with published normative values and investigated whether CHD groups differ from each other in terms of head circumference (HC) development over gestational age (GA). Materials and Methods Retrospective cohort study consisting of 248 CHD fetuses. Subgroups were generated according to the expected ascending aorta oxygen saturation: Low placental blood content (BC) and therefore low oxygen delivery to the brain (group 1: n = 108), intermediate placental and systemic BC due to intracardiac mixing of blood (group 2: n = 103), high placental BC (group 3: n = 13) and low placental BC and low oxygen delivery to the brain without mixing of blood (group 4: n = 24). Furthermore, group 1 was divided into antegrade (n = 34) and retrograde (n = 74) flow through the aortic arch. Comparisons were made at a GA of 22, 30 and 38 weeks. Results Estimated values of zHC (z-score transformed) were not significantly different between the four CHD groups at the three time points in gestation (all p > 0.05). Within group 1 fetuses with retrograde aortic arch flow showed a significant negative association between HC and GA compared to reference values (b = –0.054, p < 0.001) and had significantly lower zHC values at 38 weeks (–0.836) compared to fetuses with antegrade flow (0.366, p = 0.009). Conclusion Our data do not confirm that CHD fetuses in general have a significantly smaller HC. HC becomes smaller throughout gestation depending on the direction of aortic arch flow.

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“…Abnormal placentation is seen in both fetuses and gravidas with CHD. Rychik et al in a single‐center cohort study found that fetuses with complex CHD had significant placental pathology, including low placental‐to‐birth weight ratio, abnormal chorangiosis, hypomature villi, thrombosis, and infarction (Rychik et al, ). Conversely, women with CHD are more likely to have abnormal uteroplacental blood flow examined by Doppler ultrasound suggestive of abnormal placentation (Balci et al, ; Pieper et al, ).…”

Section: Association Of Human Chd With Early Onset Placental Insufficmentioning

confidence: 99%

Oxygen and lack of oxygen in fetal and placental development, feto–placental coupling, and congenital heart defects

Olivé

Xiao

Natale

et al. 2018

Birth Defects Research

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Low oxygen concentration (hypoxia) is part of normal embryonic development, yet the situation is complex. Oxygen (O2) is a janus gas with low levels signaling through hypoxia‐inducible transcription factor (HIF) that are required for development of fetal and placental vasculature and fetal red blood cells. This results in coupling of fetus and mother around midgestation as a functional feto‐placental unit (FPU) for O2 transport, which is required for continued growth and development of the fetus. Defects in these processes may leave the developing fetus vulnerable to O2 deprivation or other stressors during this critical midgestational transition when common septal and conotruncal heart defects (CHDs) are likely to arise. Recent human epidemiological and case–control studies support an association between placental dysfunction, manifest as early onset pre‐eclampsia (PE) and increased serum bio‐markers, and CHD. Animal studies support this association, in particular those using gene inactivation in the mouse. Sophisticated methods for gene inactivation, cell fate mapping, and a quantitative bio‐reporter of O2 concentration support the premise that hypoxic stress at critical stages of development leads to CHD. The secondary heart field contributing to the cardiac outlet is a key target, with activation of the un‐folded protein response and abrogation of FGF signaling or precocious activation of a cardiomyocyte transcriptional program for differentiation, suggested as mechanisms. These studies provide a strong foundation for further study of feto–placental coupling and hypoxic stress in the genesis of human CHD.

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Characterization of the Placenta in the Newborn with Congenital Heart Disease: Distinctions Based on Type of Cardiac Malformation

Cited by 101 publications

References 31 publications

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

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

Head Biometry in Fetuses with Isolated Congenital Heart Disease

Oxygen and lack of oxygen in fetal and placental development, feto–placental coupling, and congenital heart defects

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