Evidence map›Paper›PMID 28062416›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2017

Blood flow patterns underlie developmental heart defects.

Madeline Midgett, Kent Thornburg, Sandra Rugonyi

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Feto-placental blood vessel development.Development (Cambridge, England) · 2025
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Effect of vinpocetine on embryonic heart rateCurrent research in toxicology · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Preeclampsia and Fetal Congenital Heart Defects.Current cardiology reviews · 2022
    Review
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

3 authors at 1 institution in 1 country.

Madeline MidgettBiomedical Engineering, Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon; and.
Kent ThornburgCenter for Developmental Health, Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon.
Sandra RugonyiBiomedical Engineering, Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon; and rugonyis@ohsu.edu.
Oregon Health & Science University · US

Funding

ULTRASOUND IMAGING COREP01HD034430 · NICHD · OREGON HEALTH & SCIENCE UNIVERSITY · PI THOMAS, GEORGE VICTOR · 1997 to 2017
$20.7M
Dynamic changes in the chick developing heart in response to altered hemodynamicsR01HL094570 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI RUGONYI, SANDRA · 2009 to 2017
$3.8M
NHLBI NIH HHS R01 HL094570NICHD NIH HHS P01 HD034430
6 · The paper itself

Abstract

Although cardiac malformations at birth are typically associated with genetic anomalies, blood flow dynamics also play a crucial role in heart formation. However, the relationship between blood flow patterns in the early embryo and later cardiovascular malformation has not been determined. We used the chicken embryo model to quantify the extent to which anomalous blood flow patterns predict cardiac defects that resemble those in humans and found that restricting either the inflow to the heart or the outflow led to reproducible abnormalities with a dose-response type relationship between blood flow stimuli and the expression of cardiac phenotypes. Constricting the outflow tract by 10-35% led predominantly to ventricular septal defects, whereas constricting by 35-60% most often led to double outlet right ventricle. Ligation of the vitelline vein caused mostly pharyngeal arch artery malformations. We show that both cardiac inflow reduction and graded outflow constriction strongly influence the development of specific and persistent abnormal cardiac structure and function. Moreover, the hemodynamic-associated cardiac defects recapitulate those caused by genetic disorders. Thus our data demonstrate the importance of investigating embryonic blood flow conditions to understand the root causes of congenital heart disease as a prerequisite to future prevention and treatment.

Indexed as

Coronary CirculationAnimalsArteriesBlood Flow VelocityBranchial RegionChick EmbryoChickensFetusHeart Defects, CongenitalHeart Septal Defects, VentricularHeart VentriclesHemodynamicsPhenotypeRegional Blood FlowTomography, X-Ray Computedchick embryocongenital heart defectshemodynamicsoutflow tract bandingvitelline vein ligation

Identifiers

PMID28062416
PMCPMC5402020
OpenAlexW2570822001

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.