Evidence map›Paper›PMID 23023871›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Altered hemodynamics, endothelial function, and protein expression occur with aortic coarctation and persist after repair.

Arjun Menon, Thomas J Eddinger, Hongfeng Wang, David C Wendell, Jeffrey M Toth, John F LaDisa

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 47 citations in OpenAlex.

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  12. Clinical, Experimental, and Computational Validation of a New Doppler-Based Index for Coarctation Severity Assessment.Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography · 2022
    Article
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  17. Predictive factors for residual hypertension following aortic coarctation stenting.Journal of clinical hypertension (Greenwich, Conn.) · 2019
    Article
  18. Computational Fluid Dynamics of Vascular Disease in Animal Models.Journal of biomechanical engineering · 2018
    Review
  19. Article
  20. 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

6 authors at 4 institutions in 1 country.

Arjun MenonDepartment of Biomedical Engineering, Marquette University, Milwaukee, WI, USA.
Thomas J Eddinger
Hongfeng Wang
David C Wendell
Jeffrey M Toth
John F LaDisa
Marquette University · USChildren's Hospital of Wisconsin · USDuke University · USMedical College of Wisconsin · US

Funding

Quantifying altered hemodynamics in response to stenting for aortic coarctationR15HL096096 · NHLBI · MARQUETTE UNIVERSITY · PI LADISA, JOHN FRANK · 2009 to 2009
$228k
NHLBI NIH HHS R15-HL-096096-01
6 · The paper itself

Abstract

Coarctation of the aorta (CoA) is associated with substantial morbidity despite treatment. Mechanically induced structural and functional vascular changes are implicated; however, their relationship with smooth muscle (SM) phenotypic expression is not fully understood. Using a clinically representative rabbit model of CoA and correction, we quantified mechanical alterations from a 20-mmHg blood pressure (BP) gradient in the thoracic aorta and related the expression of key SM contractile and focal adhesion proteins with remodeling, relaxation, and stiffness. Systolic and mean BP were elevated for CoA rabbits compared with controls leading to remodeling, stiffening, an altered force response, and endothelial dysfunction both proximally and distally. The proximal changes persisted for corrected rabbits despite >12 wk of normal BP (~4 human years). Computational fluid dynamic simulations revealed reduced wall shear stress (WSS) proximally in CoA compared with control and corrected rabbits. Distally, WSS was markedly increased in CoA rabbits due to a stenotic velocity jet, which has persistent effects as WSS was significantly reduced in corrected rabbits. Immunohistochemistry revealed significantly increased nonmuscle myosin and reduced SM myosin heavy chain expression in the proximal arteries of CoA and corrected rabbits but no differences in SM α-actin, talin, or fibronectin. These findings indicate that CoA can cause alterations in the SM phenotype contributing to structural and functional changes in the proximal arteries that accompany the mechanical stimuli of elevated BP and altered WSS. Importantly, these changes are not reversed upon BP correction and may serve as markers of disease severity, which explains the persistent morbidity observed in CoA patients.

Indexed as

Cardiovascular Surgical ProceduresActinsAnimalsAortic CoarctationBlood PressureContractile ProteinsEndothelium, VascularFibronectinsHemodynamicsMaleModels, AnimalMyosin Heavy ChainsRabbitsShear StrengthStress, MechanicalTalinActinsContractile ProteinsFibronectinsMyosin Heavy ChainsTalin

Identifiers

PMID23023871
PMCPMC3532538
OpenAlexW1978828413

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.