Evidence map›Paper›PMID 30958237›Full record

ArticleJournal of the Royal Society, Interface2018

Particle-based computational modelling of arterial disease.

H Ahmadzadeh, M K Rausch, J D Humphrey

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Complementary roles of mechanotransduction and inflammation in vascular homeostasis.Proceedings. Mathematical, physical, and engineering sciences · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Central artery stiffness and thoracic aortopathy.American journal of physiology. Heart and circulatory physiology · 2019
    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 2 institutions in 1 country.

H Ahmadzadeh1 Department of Biomedical Engineering, Yale University , New Haven, CT , USA.
M K Rausch2 Departments of Aerospace Engineering and Engineering Mechanics and Biomedical Engineering, The University of Texas at Austin , Austin, TX , USA.
J D Humphrey1 Department of Biomedical Engineering, Yale University , New Haven, CT , USA.
Yale University · USThe University of Texas at Austin · US

Funding

TGFB-Dependent Mechanoresponses by Aortic Smooth Muscle Cells Govern AneurysmsP01HL134605 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUMPHREY, JAY D. · 2018 to 2022
$12.1M
Multimodality imaging-driven multifidelity modeling of aortic dissectionU01HL142518 · NHLBI · YALE UNIVERSITY · PI HUMPHREY, JAY D., KARNIADAKIS, GEORGE · 2018 to 2022
$2.8M
Multiscale, Multiphysics Model of Thrombus Biomechanics in Aortic DissectionU01HL116323 · NHLBI · YALE UNIVERSITY · PI HUMPHREY, JAY D., KARNIADAKIS, GEORGE · 2013 to 2017
$2.4M
A new paradigm for aortic dissection: Mechanical mechanisms of delaminationR21EB020968 · NIBIB · YALE UNIVERSITY · PI HUMPHREY, JAY D. · 2016 to 2017
$461k
NHLBI NIH HHS P01 HL134605NHLBI NIH HHS U01 HL116323NHLBI NIH HHS U01 HL142518NIBIB NIH HHS R21 EB020968
6 · The paper itself

Abstract

Accumulated glycosaminoglycans (GAGs) can sequester water and induce swelling within the intra-lamellar spaces of the medial layer of an artery. It is increasingly believed that stress concentrations caused by focal swelling can trigger the damage and delamination that is often seen in thoracic aortic disease. Here, we present computational simulations using an extended smoothed particle hydrodynamics approach to examine potential roles of pooled GAGs in initiating and propagating intra-lamellar delaminations. Using baseline models of the murine descending thoracic aorta, we first calculate stress distributions in a healthy vessel. Next, we examine increases in mechanical stress in regions surrounding GAG pools. The simulations show that smooth muscle activation can partially protect the wall from swelling-associated damage, consistent with experimental observations, but the wall can yet delaminate particularly in cases of smooth muscle dysfunction or absence. Moreover, pools of GAGs located at different but nearby locations can extend and coalesce, thus propagating a delamination. These findings, combined with a sensitivity study on the input parameters of the model, suggest that localized swelling can alter aortic mechanics in ways that eventually can cause catastrophic damage within the wall. There is, therefore, an increased need to consider roles of GAGs in aortic pathology.

Indexed as

Aorta, ThoracicComputer SimulationModels, CardiovascularVascular DiseasesAnimalsGlycosaminoglycansMiceGlycosaminoglycansaortic dissectionDonnan swellingglycosaminoglycanssmoothed particle hydrodynamicssoft tissue

Identifiers

PMID30958237
PMCPMC6303797
OpenAlexW2904964614

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.