Literature DB >> 32927345

Abnormalities of placental development and function are associated with the different fetal growth patterns of hypoplastic left heart syndrome and transposition of the great arteries.

Jennifer Courtney1, Weston Troja1, Kathryn J Owens1, Heather M Brockway2, Andrea C Hinton3, Robert B Hinton3, James F Cnota4, Helen N Jones5.   

Abstract

BACKGROUND: Birthweight is a critical predictor of congenital heart disease (CHD) surgical outcomes. Hypoplastic left heart syndrome (HLHS) is cyanotic CHD with known fetal growth restriction and placental abnormalities. Transposition of the great arteries (TGA) is cyanotic CHD with normal fetal growth. Comparison of the placenta in these diagnoses may provide insights on the fetal growth abnormality of CHD.
METHODS: Clinical data and placental histology from placentas associated with Transposition of the Great Arteries (TGA) were analyzed for gross pathology, morphology, maturity and vascularity and compared to both control and previously analyzed HLHS placentas [1]. RNA was isolated from HLHS, TGA and control placentas and sequenced by Illumina HiSeq.Transcriptome analysis was performed using AltAnalyze. Immunohistochemistry was utilized to assess placental nutrient transporter expression in all three groups.
RESULTS: Placental weight was reduced in TGA cases, and demonstrated reduced villous vasculature, immature terminal villi in the parenchyma compared to controls and reflected our previous data from HLHS placentas. However, birth weight was not reduced in TGA cases compared to controls in contrast to the HLHS cohort and birthweight:placental weight ratio was significantly increased in TGA cases but not HLHS compared to control. Transcriptomic and histologic analysis demonstrates reduced cell activity and nutrient transport capability in HLHS but not TGA placentas which appear to increase/maintain these mechanisms.
CONCLUSIONS: Despite common vascular disturbances in placentas from HLHAs and TGA, these do not account for the disparities in birthweights frequently seen between these CHD subtypes, in contrast our transcriptomic and histologic analyses reveal differentially regulated mechanisms between the subtypes that may explain these disparities.
Copyright © 2020 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Congenital heart defects; Fetal growth; Nutrient transporters; Placental transcriptome

Year:  2020        PMID: 32927345     DOI: 10.1016/j.placenta.2020.09.007

Source DB:  PubMed          Journal:  Placenta        ISSN: 0143-4004            Impact factor:   3.481


  4 in total

1.  Analysis of Placental Arteriovenous Formation Reveals New Insights Into Embryos With Congenital Heart Defects.

Authors:  Jacinta I Kalisch-Smith; Emily C Morris; Mary A A Strevens; Andia N Redpath; Kostantinos Klaourakis; Dorota Szumska; Jennifer E Outhwaite; Xin Sun; Joaquim Miguel Vieira; Nicola Smart; Sarah De Val; Paul R Riley; Duncan B Sparrow
Journal:  Front Genet       Date:  2022-01-19       Impact factor: 4.599

2.  The Effect of Size and Asymmetry at Birth on Brain Injury and Neurodevelopmental Outcomes in Congenital Heart Disease.

Authors:  Shalin A Parekh; Stephany M Cox; A James Barkovich; Vann Chau; Martina A Steurer; Duan Xu; Steven P Miller; Patrick S McQuillen; Shabnam Peyvandi
Journal:  Pediatr Cardiol       Date:  2021-12-01       Impact factor: 1.655

Review 3.  Neuroplacentology in congenital heart disease: placental connections to neurodevelopmental outcomes.

Authors:  Rachel L Leon; Imran N Mir; Christina L Herrera; Kavita Sharma; Catherine Y Spong; Diane M Twickler; Lina F Chalak
Journal:  Pediatr Res       Date:  2021-04-16       Impact factor: 3.953

Review 4.  Birthweight and isolated congenital heart defects - A systematic review and meta-analysis.

Authors:  Moska Aliasi; Maartje C Snoep; Nan van Geloven; Monique C Haak
Journal:  BJOG       Date:  2022-04-15       Impact factor: 7.331

  4 in total

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