Evidence map›Paper›PMID 17599600›Full record

ReviewJournal of the American College of Cardiology2007

Role of endothelial shear stress in the natural history of coronary atherosclerosis and vascular remodeling: molecular, cellular, and vascular behavior.

Yiannis S Chatzizisis, Ahmet Umit Coskun, Michael Jonas, Elazer R Edelman, Charles L Feldman, Peter H Stone

2 registry-linked trialsAbstract readReview
PubMed Publisher
In one paragraph

Review in Journal of the American College of Cardiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 549 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
549citing papers in PubMed, 4 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.

NCT03829046 phase4completedstarted 2019, after this paper: background citation

The Effects of Evolocumab on Endothelial and Inflammatory Biocellular Markers in Patients With Diabetes and Atherosclerotic Vascular Disease (METCHNIKOFF)

Ran2019Enrolled41Registered outcomes11Posted comparisons0ConditionsAtherosclerotic Vascular Disease, Microvascular Dysfunction, Type2 DiabetesArmsEvolocumab, Placebo
Open the trial in the graph
NCT03033810 unknown statusnot on this mapstarted 2017, after this paper: background citation

FFR Versus iFR in Assessment of Hemodynamic Lesion Significance Using Gene Polymorphisms and Lesion Morphology Assessed by OCT (FiGARO Trial)

TypeobservationalSponsorGeneral University Hospital, PragueRan2017 to 2019Enrolled200ConditionsHemodynamics, Coronary Circulation, Tomography, Optical Coherence, Endothelial CellsArmsFractional flow reserve and instantaneous wave-free ratio
3 · Its place in the literature

Who cites it

549 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  4. Profiling cerebrovascular function in migraine: A systematic review and meta-analysis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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489 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Yiannis S ChatzizisisCardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Ahmet Umit Coskun
Michael Jonas
Elazer R Edelman
Charles L Feldman
Peter H Stone

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the entire coronary tree is exposed to the atherogenic effect of the systemic risk factors, atherosclerotic lesions form at specific arterial regions, where low and oscillatory endothelial shear stress (ESS) occur. Low ESS modulates endothelial gene expression through complex mechanoreception and mechanotransduction processes, inducing an atherogenic endothelial phenotype and formation of an early atherosclerotic plaque. Each early plaque exhibits an individual natural history of progression, regression, or stabilization, which is dependent not only on the formation and progression of atherosclerosis but also on the vascular remodeling response. Although the pathophysiologic mechanisms involved in the remodeling of the atherosclerotic wall are incompletely understood, the dynamic interplay between local hemodynamic milieu, low ESS in particular, and the biology of the wall is likely to be important. In this review, we explore the molecular, cellular, and vascular processes supporting the role of low ESS in the natural history of coronary atherosclerosis and vascular remodeling and indicate likely mechanisms concerning the different natural history trajectories of individual coronary lesions. Atherosclerotic plaques associated with excessive expansive remodeling evolve to high-risk plaques, because low ESS conditions persist, thereby promoting continued local lipid accumulation, inflammation, oxidative stress, matrix breakdown, and eventually further plaque progression and excessive expansive remodeling. An enhanced understanding of the pathobiologic processes responsible for atherosclerosis and vascular remodeling might allow for early identification of a high-risk coronary plaque and thereby provide a rationale for innovative diagnostic and/or therapeutic strategies for the management of coronary patients and prevention of acute coronary syndromes.

Indexed as

Blood Flow VelocityCoronary Artery DiseaseCoronary CirculationCoronary VesselsDisease ProgressionEndothelium, VascularFemaleHumansMaleMechanoreceptorsNitric OxideNitric Oxide Synthase Type IIIOxidative StressRegenerationRisk AssessmentSensitivity and SpecificityNitric OxideNitric Oxide Synthase Type IIINOS3 protein, human

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.