Evidence map›Paper›PMID 27055190›Full record

ReviewPediatric research2016

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

Abraham M Rudolph

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Pediatric research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.3field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Fetal Cerebral Blood Flow (Dys)autoregulation.Diagnostics (Basel, Switzerland) · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Total and Regional Brain Volumes in Fetuses With Congenital Heart Disease.Journal of magnetic resonance imaging : JMRI · 2024
    Article
  7. Article
  8. Review
  9. Fetal brain issues in congenital heart disease.Translational pediatrics · 2021
    Review
  10. Fetal cerebrovascular response to maternal hyperoxygenation in congenital heart disease: effect of cardiac physiology.Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Observational
  17. Placental MRI: Developing Accurate Quantitative Measures of Oxygenation.Topics in magnetic resonance imaging : TMRI · 2019
    Review
  18. Article
  19. Growth patterns and cerebroplacental hemodynamics in fetuses with congenital heart disease.Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology · 2019
    Article
  20. Chronic intrauterine hypoxia alters neurodevelopment in fetal sheep.The Journal of thoracic and cardiovascular surgery · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Abraham M RudolphDepartment of Pediatrics, University of California San Francisco, San Francisco, California.
University of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AortaBlood GlucoseBody WeightBrainBrain DiseasesCardiovascular SystemCerebrovascular CirculationFemaleGestational AgeGlucoseHeart Defects, CongenitalHemodynamicsHumansHypoplastic Left Heart SyndromeHypoxiaMiddle Cerebral ArteryBlood GlucoseGlucoseOxygen

Identifiers

PMID27055190
OpenAlexW2325043769

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.