Evidence map›Paper›PMID 26822720›Full record

ReviewNature reviews. Cardiology2016

Role of biomechanical forces in the natural history of coronary atherosclerosis.

Adam J Brown, Zhongzhao Teng, Paul C Evans, Jonathan H Gillard, Habib Samady, Martin R Bennett

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed
26.7field-weighted citation impact, top 1% 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

126 citing papers in PubMed, 263 citations in OpenAlex.

  1. Article
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  5. Hemodynamic Metrics and Arterial Dysfunction: Insights From a Novel Microfluidic Device.International journal for numerical methods in biomedical engineering · 2026
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  7. Review
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  14. Smoking and Coronary Atherosclerosis: Disproportionate Impact on the Right Coronary Artery.Journal of the Society for Cardiovascular Angiography & Interventions · 2025
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

66 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 2 countries.

Adam J BrownDivision of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
Zhongzhao TengDepartment of Radiology, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
Paul C EvansDepartment of Cardiovascular Science, University of Sheffield, Western Bank, Sheffield S10 2TN, UK.
Jonathan H GillardDepartment of Radiology, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
Habib SamadyDepartment of Medicine, Emory University, 100 Woodruff Circle, Atlanta, Georgia 30322, USA.
Martin R BennettDivision of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
Addenbrooke's Hospital · GBEmory University · USUniversity of Cambridge · GBUniversity of Sheffield · GB

Funding

British Heart Foundation FS/13/27/30191British Heart Foundation FS/13/33/30168British Heart Foundation FS/15/26/31441British Heart Foundation PG/11/74/29100British Heart Foundation RG/10/007/28300British Heart Foundation RG/13/1/30042Medical Research Council G0800784Medical Research Council G1000847Medical Research Council MC_PC_14116
6 · The paper itself

Abstract

Atherosclerosis remains a major cause of morbidity and mortality worldwide, and a thorough understanding of the underlying pathophysiological mechanisms is crucial for the development of new therapeutic strategies. Although atherosclerosis is a systemic inflammatory disease, coronary atherosclerotic plaques are not uniformly distributed in the vascular tree. Experimental and clinical data highlight that biomechanical forces, including wall shear stress (WSS) and plaque structural stress (PSS), have an important role in the natural history of coronary atherosclerosis. Endothelial cell function is heavily influenced by changes in WSS, and longitudinal animal and human studies have shown that coronary regions with low WSS undergo increased plaque growth compared with high WSS regions. Local alterations in WSS might also promote transformation of stable to unstable plaque subtypes. Plaque rupture is determined by the balance between PSS and material strength, with plaque composition having a profound effect on PSS. Prospective clinical studies are required to ascertain whether integrating mechanical parameters with medical imaging can improve our ability to identify patients at highest risk of rapid disease progression or sudden cardiac events.

Indexed as

Coronary CirculationAnimalsBiomechanical PhenomenaCoronary Artery DiseaseCoronary VesselsDisease ProgressionHumansPlaque, AtheroscleroticPrognosisRupture, SpontaneousSignal TransductionStress, Mechanical

Identifiers

PMID26822720
OpenAlexW2281289255

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.