Evidence map›Paper›PMID 34740008›Full record

ArticleJournal of the mechanical behavior of biomedical materials2022

Finite element analysis in clinical patients with atherosclerosis.

Christopher Noble, Kent D Carlson, Erica Neumann, Bradley Lewis, Dan Dragomir-Daescu, Amir Lerman, Ahmet Erdemir, Melissa D Young

Abstract read
In one paragraph

Article in Journal of the mechanical behavior of biomedical materials, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Observational
  2. Biomechanical stress profiling in coronary arteries via two-phase blood FSI.Biomechanics and modeling in mechanobiology · 2025
    Article
  3. Article
  4. Review
  5. 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

8 authors.

Christopher NobleDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Kent D CarlsonDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA.
Erica NeumannDepartment of Biomedical Engineering and Computational Biomodeling (CoBi) Core, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Bradley LewisDivision of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, MN, USA.
Dan Dragomir-DaescuDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA.
Amir LermanDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Ahmet ErdemirDepartment of Biomedical Engineering and Computational Biomodeling (CoBi) Core, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Melissa D YoungDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA. Electronic address: young.melissa@mayo.edu.

Funding

Mayo Clinic Center for Clinical and Translational Science (CCaTS UL1 Supplement - Dr. Timothy Curry)UL1TR002377 · NCATS · MAYO CLINIC ROCHESTER · PI VESNA D GAROVIC · 2017 to 2026
$78.4M
Automated patient specific artery modeling using ultrasound virtual histologyR01EB018965 · NIBIB · MAYO CLINIC ROCHESTER · PI YOUNG, MELISSA DENTON · 2016 to 2019
$1.7M
NCATS NIH HHS UL1 TR002377NIBIB NIH HHS R01 EB018965
6 · The paper itself

Abstract

Endovascular plaque composition is strongly related to stent strut stress and is responsible for strut fatigue, stent failure, and possible in-stent restenosis. To evaluate the effect of plaque on artery wall resistance to expansion we performed in silico analysis of atherosclerotic vessels. We generated finite element models from in vivo intravascular ultrasound virtual histology images to determine local artery surface stiffness and determined which plaque structures have the greatest influence. We validated the predictive capacity of our modeling approach by testing an atherosclerotic peripheral artery ex vivo with pressure-inflation testing at physiological pressures ranging from 10 to 200 mmHg. For this purpose, the in silico deformation of the arterial wall was compared to that observed ex vivo. We found that calcification had a positive effect on surface stiffness with fibrous plaque and necrotic core having negative effects. Additionally, larger plaque structures demonstrated significantly higher average surface stiffness and calcification located nearer the lumen was also shown to increase surface stiffness. Therefore, more developed plaques will have greater resistance to expansion and higher stent strut stress, with calcification located near the lumen further increasing stress in localized areas. Thus, it may be expected that such plaque structures may increase the likelihood of localized stent strut fracture.

Indexed as

AtherosclerosisFinite Element AnalysisHumansAtherosclerosisFinite element analysisIntravascular ultrasound virtual histologyPressure-inflation testingSurface stiffness

Identifiers

PMID34740008
PMCPMC8665142

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Registered trials

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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.