Evidence mapPaperPMID 28148771Full record

Trial reportJournal of the Royal Society, Interface2017

Oscillatory wall shear stress is a dominant flow characteristic affecting lesion progression patterns and plaque vulnerability in patients with coronary artery disease.

Lucas H Timmins, David S Molony, Parham Eshtehardi, Michael C McDaniel, John N Oshinski, Don P Giddens, Habib Samady

Abstract readClinical Trial
In one paragraph

Trial report in Journal of the Royal Society, Interface, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

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

  1. Pooled it
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  6. Review
  7. Biomechanics of Plaque Rupture and Cardiovascular Calcification.Advances in experimental medicine and biology · 2026
    Review
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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

7 authors.

Lucas H TimminsDepartment of Radiology and Imaging Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA lucas.timmins@utah.edu.ORCID 0000-0002-8707-8120
David S MolonyDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Parham EshtehardiDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Michael C McDanielDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
John N OshinskiDepartment of Radiology and Imaging Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA.
Don P GiddensWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA 30322, USA.
Habib SamadyDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although experimental studies suggest that low and oscillatory wall shear stress (WSS) promotes plaque transformation to a more vulnerable phenotype, this relationship has not been examined in human atherosclerosis progression. Thus, the aim of this investigation was to examine the association between oscillatory WSS, in combination with WSS magnitude, and coronary atherosclerosis progression. We hypothesized that regions of low and oscillatory WSS will demonstrate progression towards more vulnerable lesions, while regions exposed to low and non-oscillatory WSS will exhibit progression towards more stable lesions. Patients (n = 20) with non-flow-limiting coronary artery disease (CAD) underwent baseline and six-month follow-up angiography, Doppler velocity and radiofrequency intravascular ultrasound (VH-IVUS) acquisition. Computational fluid dynamics models were constructed to compute time-averaged WSS magnitude and oscillatory WSS. Changes in VH-IVUS-defined total plaque and constituent areas were quantified in focal regions (i.e. sectors; n = 14 235) and compared across haemodynamic categories. Compared with sectors exposed to low WSS magnitude, high WSS sectors demonstrated regression of total plaque area (p < 0.001) and fibrous tissue (p < 0.001), and similar progression of necrotic core. Sectors subjected to low and oscillatory WSS exhibited total plaque area regression, while low and non-oscillatory WSS sectors demonstrated total plaque progression (p < 0.001). Furthermore, compared with low and non-oscillatory WSS areas, sectors exposed to low and oscillatory WSS demonstrated regression of fibrous (p < 0.001) and fibrofatty (p < 0.001) tissue and similar progression of necrotic core (p = 0.82) and dense calcium (p = 0.40). Herein, we demonstrate that, in patients with non-obstructive CAD, sectors subjected to low and oscillatory WSS demonstrated regression of total plaque, fibrous and fibrofatty tissue, and progression of necrotic core and dense calcium, which suggest a transformation to a more vulnerable phenotype.

Indexed as

Biological ClocksComputer SimulationModels, CardiovascularBlood Flow VelocityCoronary AngiographyCoronary Artery DiseaseEchocardiography, Doppler, ColorFemaleHumansMalePlaque, Atheroscleroticatherosclerosiscomputational fluid dynamicscoronary artery diseasehaemodynamicsintravascular ultrasoundwall shear stress

Identifiers

PMID28148771
PMCPMC5332583

What Socratic 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 Socratic graph.