Evidence map›Paper›PMID 27943104›Full record

ArticleMedical & biological engineering & computing2017

Stress analysis of fracture of atherosclerotic plaques: crack propagation modeling.

Alireza Rezvani-Sharif, Mohammad Tafazzoli-Shadpour, Davood Kazemi-Saleh, Maryam Sotoudeh-Anvari

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Article in Medical & biological engineering & computing, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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0cells of the map it votes in
4citing papers in PubMed
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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

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. [Numerical simulation study of fracture mechanics of the atherosclerotic plaque].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2021
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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Alireza Rezvani-SharifCardiovascular Engineering Lab, Faculty of Biomedical Engineering, Amirkabir University of Technology (Tehran Polytechnic), Tehran, Iran.
Mohammad Tafazzoli-ShadpourCardiovascular Engineering Lab, Faculty of Biomedical Engineering, Amirkabir University of Technology (Tehran Polytechnic), Tehran, Iran. tafazoli@aut.ac.ir.
Davood Kazemi-SalehAtherosclerosis Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
Maryam Sotoudeh-AnvariDepartment of Surgical and Clinical Pathology, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traditionally, the degree of luminal obstruction has been used to assess the vulnerability of atherosclerotic plaques. However, recent studies have revealed that other factors such as plaque morphology, material properties of lesion components and blood pressure may contribute to the fracture of atherosclerotic plaques. The aim of this study was to investigate the mechanism of fracture of atherosclerotic plaques based on the mechanical stress distribution and fatigue analysis by means of numerical simulation. Realistic models of type V plaques were reconstructed based on histological images. Finite element method was used to determine mechanical stress distribution within the plaque. Assuming that crack propagation initiated at the sites of stress concentration, crack propagation due to pulsatile blood pressure was modeled. Results showed that crack propagation considerably changed the stress field within the plaque and in some cases led to initiation of secondary cracks. The lipid pool stiffness affected the location of crack formation and the rate and direction of crack propagation. Moreover, increasing the mean or pulse pressure decreased the number of cycles to rupture. It is suggested that crack propagation analysis can lead to a better recognition of factors involved in plaque rupture and more accurate determination of vulnerable plaques.

Indexed as

Models, CardiovascularComputer SimulationCoronary Artery DiseaseCoronary VesselsElastic ModulusFemaleFinite Element AnalysisHumansMaleMiddle AgedModels, AnatomicPlaque, AtheroscleroticShear StrengthStress, MechanicalAtherosclerotic plaqueFatigueFinite element methodFracture mechanicsMyocardial infarction

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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.