Evidence map›Paper›PMID 38704690›Full record

ReviewAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Integrating Computational and Biological Hemodynamic Approaches to Improve Modeling of Atherosclerotic Arteries.

Thao Nhu Anne Marie Vuong, Michael Bartolf-Kopp, Kristina Andelovic, Tomasz Jungst, Nona Farbehi, Steven G Wise, Christopher Hayward, Michael Charles Stevens, Jelena Rnjak-Kovacina

Abstract readReview
In one paragraph

Review in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–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

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. 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

9 authors.

Thao Nhu Anne Marie VuongGraduate School of Biomedical Engineering, University of New South Wales, Sydney, 2052, Australia.
Michael Bartolf-KoppDepartment of Functional Materials in Medicine and Dentistry, Institute of Functional Materials and Biofabrication (IFB), KeyLab Polymers for Medicine of the Bavarian Polymer Institute (BPI), University of Würzburg, Pleicherwall 2, 97070, Würzburg, Germany.ORCID 0000-0002-8792-8914
Kristina AndelovicDepartment of Functional Materials in Medicine and Dentistry, Institute of Functional Materials and Biofabrication (IFB), KeyLab Polymers for Medicine of the Bavarian Polymer Institute (BPI), University of Würzburg, Pleicherwall 2, 97070, Würzburg, Germany.ORCID 0000-0001-8869-8359
Tomasz JungstDepartment of Functional Materials in Medicine and Dentistry, Institute of Functional Materials and Biofabrication (IFB), KeyLab Polymers for Medicine of the Bavarian Polymer Institute (BPI), University of Würzburg, Pleicherwall 2, 97070, Würzburg, Germany.ORCID 0000-0002-2458-8713
Nona FarbehiGraduate School of Biomedical Engineering, University of New South Wales, Sydney, 2052, Australia.ORCID 0000-0001-8461-236X
Steven G WiseSchool of Medical Sciences, University of Sydney, Sydney, NSW, 2006, Australia.ORCID 0000-0001-7964-819X
Christopher HaywardSt Vincent's Hospital, Sydney, Victor Chang Cardiac Research Institute, Sydney, 2010, Australia.
Michael Charles StevensGraduate School of Biomedical Engineering, University of New South Wales, Sydney, 2052, Australia.ORCID 0000-0003-3583-688X
Jelena Rnjak-KovacinaGraduate School of Biomedical Engineering, University of New South Wales, Sydney, 2052, Australia.ORCID 0000-0001-6121-4676

Funding

Australian Research Council FT210100668National Heart Foundation Future Leader Fellowship 105622University of New South Wales Scientia Program
6 · The paper itself

Abstract

Atherosclerosis is the primary cause of cardiovascular disease, resulting in mortality, elevated healthcare costs, diminished productivity, and reduced quality of life for individuals and their communities. This is exacerbated by the limited understanding of its underlying causes and limitations in current therapeutic interventions, highlighting the need for sophisticated models of atherosclerosis. This review critically evaluates the computational and biological models of atherosclerosis, focusing on the study of hemodynamics in atherosclerotic coronary arteries. Computational models account for the geometrical complexities and hemodynamics of the blood vessels and stenoses, but they fail to capture the complex biological processes involved in atherosclerosis. Different in vitro and in vivo biological models can capture aspects of the biological complexity of healthy and stenosed vessels, but rarely mimic the human anatomy and physiological hemodynamics, and require significantly more time, cost, and resources. Therefore, emerging strategies are examined that integrate computational and biological models, and the potential of advances in imaging, biofabrication, and machine learning is explored in developing more effective models of atherosclerosis.

Indexed as

AtherosclerosisHemodynamicsAnimalsComputer SimulationHumansModels, Cardiovascularatherosclerosiscardiovascular diseasecomputational modelinghaemodynamicstissue engineering

Identifiers

PMID38704690
PMCPMC11234431

What OpenQuestion holds

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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.