Evidence map›Paper›PMID 28275592›Full record

ArticleFrontiers in pediatrics2017

Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape.

Sukriti Dewan, Adarsh Krishnamurthy, Devleena Kole, Giulia Conca, Roy Kerckhoffs, Michael D Puchalski, Jeffrey H Omens, Heather Sun, Vishal Nigam, Andrew D McCulloch

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pediatrics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Effects of cardiac growth on electrical dyssynchrony in the single ventricle patient.Computer methods in biomechanics and biomedical engineering · 2024
    Article
  3. Review
  4. Article
  5. Article
  6. Mending a broken heart:Disease models & mechanisms · 2021
    Review
  7. Article
  8. 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

10 authors at 4 institutions in 1 country.

Sukriti DewanDepartment of Bioengineering, University of California at San Diego , La Jolla, CA , USA.
Adarsh KrishnamurthyDepartment of Bioengineering, University of California at San Diego, La Jolla, CA, USA; Department of Mechanical Engineering, Iowa State University, Ames, IA, USA.
Devleena KoleDepartment of Bioengineering, University of California at San Diego , La Jolla, CA , USA.
Giulia ConcaDepartment of Bioengineering, University of California at San Diego , La Jolla, CA , USA.
Roy KerckhoffsDepartment of Bioengineering, University of California at San Diego , La Jolla, CA , USA.
Michael D PuchalskiPediatric Cardiology, Primary Children's Hospital, University of Utah , Salt Lake City, UT , USA.
Jeffrey H OmensDepartment of Bioengineering, University of California at San Diego, La Jolla, CA, USA; Department of Medicine, University of California at San Diego, La Jolla, CA, USA.
Heather SunPediatric Cardiology, Rady Children's Hospital, University of California at San Diego , San Diego, CA , USA.
Vishal NigamPediatric Cardiology, Rady Children's Hospital, University of California at San Diego , San Diego, CA , USA.
Andrew D McCullochDepartment of Bioengineering, University of California at San Diego, La Jolla, CA, USA; Department of Medicine, University of California at San Diego, La Jolla, CA, USA.
Rady Children's Hospital-San Diego · USUniversity of California, San Diego · USIowa State University · USPrimary Children's Hospital · US

Funding

National Biomedical Computation Resource - Competitive Revision SupplementP41GM103426 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI AMARO, ROMMIE E · 2012 to 2019
$14.0M
Analyzing the Cardiac Power Grid: Adaptive responses to fluctuating local demandU01HL122199 · NHLBI · UNIVERSITY OF WASHINGTON · PI BEARD, DANIEL A, DASH, RANJAN K · 2015 to 2019
$3.3M
Research Training in Pediatric Critical Care MedicineT32HD049303 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JEFFREY R FINEMAN · 2006 to 2026
$3.1M
Systems Biology of Hypertrophic Heart Disease from Molecular Pathways to Organ SystemR01HL137100 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MCCULLOCH, ANDREW D. · 2017 to 2020
$2.0M
A Multiscale Modeling Approach to Hypoplastic Left Heart SyndromeR01HL128630 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DEL ALAMO, JUAN CARLOS, NIGAM, VISHAL · 2016 to 2019
$1.5M
NHLBI NIH HHS R01 HL128630NHLBI NIH HHS R01 HL137100NHLBI NIH HHS U01 HL122199NICHD NIH HHS T32 HD049303NIGMS NIH HHS P41 GM103426
6 · The paper itself

Abstract

introductionHypoplastic left heart syndrome (HLHS) is a congenital condition with an underdeveloped left ventricle (LV) that provides inadequate systemic blood flow postnatally. The development of HLHS is postulated to be due to altered biomechanical stimuli during gestation. Predicting LV size at birth using mid-gestation fetal echocardiography is a clinical challenge critical to prognostic counseling. HYPOTHESIS: We hypothesized that decreased ventricular filling

methodsWe developed a novel finite element model of the human fetal heart in which cardiac myocyte growth rates are a function of fiber and cross-fiber strains, which is affected by altered ventricular filling, to simulate alterations in LV growth and remodeling. Model results were tested with echocardiogram measurements from normal and HLHS fetal hearts.

resultsA strain-based fetal growth model with a normal 22-week ventricular filling (1.04 mL) was able to replicate published measurements of changes between mid-gestation to birth of mean LV end-diastolic volume (EDV) (1.1-8.3 mL) and dimensions (long-axis, 18-35 mm; short-axis, 9-18 mm) within 15% root mean squared deviation error. By decreasing volumetric load (-25%) at mid-gestation in the model, which emulates mitral stenosis

conclusionReduced ventricular filling and altered shape may lead to reduced LV growth and a hypoplastic phenotype by reducing myocardial strains that serve as a myocyte growth stimulus. The human fetal growth model presented here may lead to a clinical tool that can help predict LV size and shape at birth based on mid-gestation LV echocardiographic measurements.

Indexed as

biomechanicscomputational modelgrowth hormoneHLHSmechanobiologypatient-specific modelingsarcomeres

Identifiers

PMID28275592
PMCPMC5319967
OpenAlexW2590587962

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.