Evidence map›Paper›PMID 24841070›Full record

ArticleCardiovascular research2014

Extent of flow recirculation governs expression of atherosclerotic and thrombotic biomarkers in arterial bifurcations.

Jordi Martorell, Pablo Santomá, Kumaran Kolandaivelu, Vijaya B Kolachalama, Pedro Melgar-Lesmes, José J Molins, Lawrence Garcia, Elazer R Edelman, Mercedes Balcells

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2014. 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
2.4field-weighted citation impact, top 10% 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, 63 citations in OpenAlex.

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  20. Pulsatility and high shear stress deteriorate barrier phenotype in brain microvascular endothelium.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
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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 at 5 institutions in 2 countries.

Jordi MartorellInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA, USA Department of Chemical Engineering, IQS School of Engineering, URL, Via Augusta 390, 08017 Barcelona, Spain jordi.martorell@iqs.edu.
Pablo SantomáInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA, USA Department of Chemical Engineering, IQS School of Engineering, URL, Via Augusta 390, 08017 Barcelona, Spain.
Kumaran KolandaiveluInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA, USA.
Vijaya B KolachalamaInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA, USA Charles Stark Draper Laboratory, Cambridge, MA, USA.
Pedro Melgar-LesmesInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA, USA.
José J MolinsDepartment of Chemical Engineering, IQS School of Engineering, URL, Via Augusta 390, 08017 Barcelona, Spain.
Lawrence GarciaDepartment of Interventional Cardiology and Vascular Medicine, St. Elizabeth's Medical Center, Boston, MA, USA.
Elazer R EdelmanInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA, USA Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Mercedes BalcellsInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA, USA Department of Biological Engineering, IQS School of Engineering, URL, Barcelona, Spain.
Institut Químic de Sarrià · ESMassachusetts Institute of Technology · USBrigham and Women's Hospital · USDraper Laboratory · USSt. Elizabeth's Medical Center · US

Funding

Vascular Drug Delivery - Supplement for EquipmentR01GM049039 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI EDELMAN, ELAZER R · 1994 to 2019
$8.9M
NIGMS NIH HHS R01 GM049039
6 · The paper itself

Abstract

aimsAtherogenesis, evolution of plaque, and outcomes following endovascular intervention depend heavily on the unique vascular architecture of each individual. Patient-specific, multiscale models able to correlate changes in microscopic cellular responses with relevant macroscopic flow, and structural conditions may help understand the progression of occlusive arterial disease, providing insights into how to mitigate adverse responses in specific settings and individuals. METHODS AND

resultsVascular architectures mimicking coronary and carotid bifurcations were derived from clinical imaging and used to generate conjoint computational meshes for in silico analysis and biocompatible scaffolds for in vitro models. In parallel with three-dimensional flow simulations, geometrically realistic scaffolds were seeded with human smooth muscle cells (SMC) or endothelial cells and exposed to relevant, physiological flows. In vitro surrogates of endothelial health, atherosclerotic progression, and thrombosis were locally quantified and correlated best with an quantified extent of flow recirculation occurring within the bifurcation models. Oxidized low-density lipoprotein uptake, monocyte adhesion, and tissue factor expression locally rose up to three-fold, and phosphorylated endothelial nitric oxide synthase and Krüppel-like factor 2 decreased up to two-fold in recirculation areas. Isolated testing in straight-tube idealized constructs subject to static, oscillatory, and pulsatile conditions, indicative of different recirculant conditions corroborated these flow-mediated dependencies.

conclusionsFlow drives variations in vascular reactivity and vascular beds. Endothelial health was preserved by arterial flow but jeopardized in regions of flow recirculation in a quasi-linear manner. Similarly, SMC exposed to flow were more thrombogenic in large recirculating regions. Health, thrombosis, and atherosclerosis biomarkers correlate with the extent of recirculation in vascular cells lining certain vascular geometries.

Indexed as

Models, CardiovascularArteriesAtherosclerosisBiomarkersBiomechanical PhenomenaCarotid ArteriesComputer SimulationCoronary VesselsDisease ProgressionEndothelial CellsHumansKruppel-Like Transcription FactorsLipoproteins, LDLMyocytes, Smooth MuscleNitric Oxide Synthase Type IIIRegional Blood FlowBiomarkersKLF2 protein, humanKruppel-Like Transcription FactorsLipoproteins, LDLNitric Oxide Synthase Type IIINOS3 protein, humanoxidized low density lipoproteinThromboplastinVascular Cell Adhesion Molecule-1AtherosclerosisEndotheliumFlowGeometryThrombosis

Identifiers

PMID24841070
PMCPMC4670884
OpenAlexW2058794464

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.