Evidence map›Paper›PMID 21398643›Full record

ReviewEuropean heart journal2011

Intraplaque haemorrhages as the trigger of plaque vulnerability.

Jean-Baptiste Michel, Renu Virmani, Eloïsa Arbustini, Gerard Pasterkamp

Registry-linked trialAbstract readReview
In one paragraph

Review in European heart journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02259257 (3D/4D Ultrasound Contrast Enhanced Imaging), which is not on this map. Cited by 145 papers.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed
–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.

NCT02259257 unknown statusnot on this mapstarted 2014, after this paper: background citation

3D/4D Ultrasound Contrast Enhanced Imaging (CEUS) for Carotid Plaque Vulnerability

TypeobservationalSponsorDiana Gaitini MD.Ran2014 to 2017Enrolled50ConditionsAtherosclerosis, Stroke
3 · Its place in the literature

Who cites it

145 citing papers in PubMed.

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  7. Multi-omics integration and machine learning identify an ACKR1Clinical and translational medicine · 2026
    Article
  8. Review
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  13. Receptor-Dependent and -Independent Effects of Hemin on Platelet Plasma Membrane Disintegration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  14. Review
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  18. Article
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85 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

4 authors.

Jean-Baptiste MichelUMR 698 Inserm, Paris 7-Denis Diderot University, Xavier Bichat Hospital, 46 rue Henri Huchard, 75018 Paris, France. jean-baptiste.michel@inserm.fr
Renu Virmani
Eloïsa Arbustini
Gerard Pasterkamp

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherothrombosis remains one of the main causes of morbidity and mortality in the western countries. Human atherothrombotic disease begins early in life in relation to circulating lipid retention in the inner vascular wall. Risk factors enhance the progression towards clinical expression: dyslipidaemia, diabetes, smoking, hypertension, ageing, etc. The evolution from the initial lipid retention in the arterial wall to clinical events is a continuum of increasingly complex biological processes. Current strategies to fight the consequences of atherothrombosis are orientated either towards the promotion of a healthy life style and preventive treatment of risk factors, or towards late interventional strategies. Despite this therapeutic arsenal, the incidence of clinical events remains dramatically high, dependent, at least in part, on the increasing frequency of type 2 diabetes and ageing. But some medical treatments, focusing only on prevention of the metabolic risk, have failed to reduce cardiovascular mortality, thus illustrating that our understanding of the pathophysiology of human atherothrombosis leading to clinical events remain incomplete. New paradigms are now emerging which may give rise to novel experimental strategies to improve therapeutic efficacy and prediction of disease progression. Recent studies strengthen the concept that the intraplaque neovascularization and bleeding (Figure 1, upper panel) are events that could play a major role in plaque progression and leucocyte infiltration, and may also serve as a measure of risk for the development of future events. The recent advances in our understanding of IntraPlaque Hemorrhage as a critical event in triggering acute clinical events have important implications for clinical research and possibly future clinical practice.

Indexed as

Angiogenesis InhibitorsBiomarkersDiagnostic ImagingEmbolism, CholesterolErythrocytesHemoglobinsHemorrhageHumansHydroxymethylglutaryl-CoA Reductase InhibitorsImmunity, CellularNeovascularization, PathologicOxidative StressPeptide HydrolasesPlaque, AtheroscleroticRisk FactorsAngiogenesis InhibitorsBiomarkersHemoglobinsHydroxymethylglutaryl-CoA Reductase InhibitorsPeptide Hydrolases

Identifiers

PMID21398643
PMCPMC3155759

What OpenQuestion holds

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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.