Placenta histology related to flow and oxygenation in fetal congenital heart disease.

Congenital heart disease Hypoplastic left heart syndrome Neurodevelopment Placenta Transposition of the great arteries

Journal

Early human development
ISSN: 1872-6232
Titre abrégé: Early Hum Dev
Pays: Ireland
ID NLM: 7708381

Informations de publication

Date de publication:
18 Jul 2024
Historique:
received: 03 06 2024
revised: 09 07 2024
accepted: 11 07 2024
medline: 26 7 2024
pubmed: 26 7 2024
entrez: 24 7 2024
Statut: aheadofprint

Résumé

Fetuses with congenital heart defects (CHD) show delayed neurodevelopment, fetal growth restriction (FGR) and placenta related complications. The neurodevelopmental delay may be, partly, attributed to placental factors. As both placental development and fetal aortic flow/oxygenation influence neurodevelopment, placentas were compared within fetal CHD groups based on aortic oxygenation and flow, aiming to unravel the true effects in the developmental processes. Placental tissues of pregnancies with fetal CHD and healthy controls were selected from biobanks of two Dutch academic hospitals (LUMC, UMCU). Additionally, biometry and Dopplers were assessed. CHD cases with reduced oxygenation (RO) towards the fetal brain were compared to cases with reduced flow (RF) in the aortic arch and healthy controls. Genetic abnormalities, termination of pregnancy, fetal demise and/or multiple pregnancies were excluded. Histological outcomes were related to fetal Dopplers and biometry. A placenta severity score was used to assess the severity of placental abnormalities per case. In CHD, significantly more delayed maturation, maternal vascular malperfusion, fetal hypoxia and higher placenta severity scores (median 14 in RO, 14 in RF, 5 in controls, p < 0.001) were observed. Doppler abnormalities (PI UA > p90, PI MCA < p10, CPR < p10) and FGR were more often found in CHD. There were no differences in placental abnormalities, fetal growth and fetal Dopplers between cases with RO and RF. Fetal hemodynamics in the ascending aorta could not be related to placenta characteristics. We hypothesize that placental development influences neurodevelopment in excess of hemodynamics in CHD cases.

Sections du résumé

BACKGROUND BACKGROUND
Fetuses with congenital heart defects (CHD) show delayed neurodevelopment, fetal growth restriction (FGR) and placenta related complications. The neurodevelopmental delay may be, partly, attributed to placental factors.
AIM OBJECTIVE
As both placental development and fetal aortic flow/oxygenation influence neurodevelopment, placentas were compared within fetal CHD groups based on aortic oxygenation and flow, aiming to unravel the true effects in the developmental processes.
STUDY DESIGN METHODS
Placental tissues of pregnancies with fetal CHD and healthy controls were selected from biobanks of two Dutch academic hospitals (LUMC, UMCU). Additionally, biometry and Dopplers were assessed.
SUBJECTS METHODS
CHD cases with reduced oxygenation (RO) towards the fetal brain were compared to cases with reduced flow (RF) in the aortic arch and healthy controls. Genetic abnormalities, termination of pregnancy, fetal demise and/or multiple pregnancies were excluded.
OUTCOME MEASURES METHODS
Histological outcomes were related to fetal Dopplers and biometry. A placenta severity score was used to assess the severity of placental abnormalities per case.
RESULTS RESULTS
In CHD, significantly more delayed maturation, maternal vascular malperfusion, fetal hypoxia and higher placenta severity scores (median 14 in RO, 14 in RF, 5 in controls, p < 0.001) were observed. Doppler abnormalities (PI UA > p90, PI MCA < p10, CPR < p10) and FGR were more often found in CHD. There were no differences in placental abnormalities, fetal growth and fetal Dopplers between cases with RO and RF.
CONCLUSION CONCLUSIONS
Fetal hemodynamics in the ascending aorta could not be related to placenta characteristics. We hypothesize that placental development influences neurodevelopment in excess of hemodynamics in CHD cases.

Identifiants

pubmed: 39047634
pii: S0378-3782(24)00148-8
doi: 10.1016/j.earlhumdev.2024.106079
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

106079

Informations de copyright

Copyright © 2024. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors have no conflicts of interest to disclose.

Auteurs

Maartje C Snoep (MC)

Department of Obstetrics and Fetal Medicine, Leiden University Medical Center, Leiden, the Netherlands. Electronic address: M.C.Snoep@lumc.nl.

Maaike Nijman (M)

Department of Neonatology, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, the Netherlands; Department of Pediatric Cardiology, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, the Netherlands.

Marco C DeRuiter (MC)

Department of Anatomy and Embryology, Leiden University Medical Center, Leiden, the Netherlands.

Mireille N Bekker (MN)

Department of Obstetrics and Fetal Medicine, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, the Netherlands.

Moska Aliasi (M)

Department of Obstetrics and Fetal Medicine, Leiden University Medical Center, Leiden, the Netherlands.

Johannes M P J Breur (JMPJ)

Department of Pediatric Cardiology, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, the Netherlands.

Arend D J Ten Harkel (ADJ)

Department of Pediatric Cardiology, Leiden University Medical Center, Leiden, the Netherlands.

Manon J N L Benders (MJNL)

Department of Neonatology, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, the Netherlands.

Lotte E van der Meeren (LE)

Department of Pathology, Leiden University Medical Center, Leiden, the Netherlands; Department of Pathology, Erasmus University Medical Center, Rotterdam, the Netherlands.

Monique C Haak (MC)

Department of Obstetrics and Fetal Medicine, Leiden University Medical Center, Leiden, the Netherlands.

Classifications MeSH