Cited by 55Congenital Heart Disease StudiesCardiovascular Conditions and TreatmentsNeonatal and fetal brain pathology

Impaired cerebral development in fetuses with congenital cardiovascular malformations: Is it the result of inadequate glucose supply?

Rudolph, Abraham M.·2016·Pediatric Research

Abstract

Cerebral development may be impaired in fetuses with congenital cardiovascular malformations, particularly hypoplastic left heart syndrome (HLHS) and aortopulmonary transposition (APT). The decreased cerebral arterial pusatility index observed in some of these fetuses led to the belief that cerebral vascular resistance was reduced as a result of arterial hypoxemia and cerebral hypoxia is thought to be responsible for impaired cerebral growth. However, other hemodynamic factors could affect pulsatility index. I propose that cerebral blood flow is reduced in fetuses with HLHS and that reduced glucose, rather than oxygen, delivery interferes with cerebral development. This is based on the fact that most of these fetuses do not have lactate accumulation in the brain.In fetuses with APT, umbilical venous blood, containing oxygen and glucose derived across the placenta, is distributed to the lungs and lower body; venous blood, with low oxygen and glucose content, is delivered to the ascending aorta and brain. Oxygen and glucose delivery may further be reduced by decreased cerebral blood flow resulting from run-off of aortic blood through the ductus arteriosus to the pulmonary circulation during diastole. In APT fetuses, lack of lactate in the brain also supports my proposal that glucose deficiency interferes with cerebral development.

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Crossref · 10.1038/pr.2016.65

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  • Chronic hypoxia likely makes brain development suboptimal, and decreased nutrient delivery such as glucose should also be considered a contributor to brain dysmaturation.

    “It is understandable that brain development will be suboptimal under conditions of chronic hypoxia, while decreased nutrient delivery (e.g.glucose) should also be considered as a contributor to brain dysmaturation.29”

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Authors
Rudolph, A. M.
Affiliations
University of California, San Francisco (US)
Corresponding author
Rudolph, Abraham M.
Venue
Pediatric Research
Published
2016-04-07
Volume
80
Issue
2
Pages
172-177
ISSN
  • 0031-3998 (ISSN-L)
  • 1530-0447
OpenAlex
W2325043769
Cited by
55
References
29
Citations by year
2026: 2 · 2025: 5 · 2024: 5 · 2023: 6 · 2022: 7 · 2021: 6 · 2020: 7 · 2019: 8 · 2018: 5 · 2017: 4
FWCI
5.32
Type
journal article
Language
en
Open access
closed
Locations
  • Pediatric Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Congenital Heart Disease Studies
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiovascular Conditions and Treatments
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
Keywords
congenital cardiovascular malformations, hypoplastic left heart syndrome, cerebral blood flow, glucose delivery, cerebral hypoxia, cerebrovascular resistance, umbilical venous blood, lactate, ductus arteriosus, fetal hemodynamics
MeSH terms
Hypoxia, Aorta, Blood Glucose, Body Weight, Brain, Brain Diseases, Cardiovascular System, Cerebrovascular Circulation, Female, Gestational Age, Glucose, Heart Defects, Congenital, Hemodynamics, Humans, Organ Size, Oxygen, Pregnancy, Time Factors, Umbilical Arteries, Hypoplastic Left Heart Syndrome, Middle Cerebral Artery

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