Evidence map›Paper›PMID 31450823›Full record

ReviewMolecules (Basel, Switzerland)2019

Immune-Mediated Inflammation in Vulnerable Atherosclerotic Plaques.

Harald Mangge, Gunter Almer

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01327846 (A Randomized, Double-blind, Placebo-controlled, Event-driven Trial of Quarterly Subcutaneous Canakinumab in the Prevention of Recurrent Cardiovascular Events Among Stable Post-myocardial Infarction Patients With Elevated hsCRP), which is not on this 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.

NCT01327846 phase3completednot on this map

A Randomized, Double-blind, Placebo-controlled, Event-driven Trial of Quarterly Subcutaneous Canakinumab in the Prevention of Recurrent Cardiovascular Events Among Stable Post-myocardial Infarction Patients With Elevated hsCRP

TypeinterventionalSponsorNovartis PharmaceuticalsRan2011 to 2019Enrolled10,066ConditionsAtherosclerosisArmsCanakinumab, Placebo, Standard of care
3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Key parameters for designing robust 2D and 3D spheroid models forBioengineering & translational medicine · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Role of oncostatin-M in ECM remodeling and plaque vulnerability.Molecular and cellular biochemistry · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Recent insights into atherosclerotic plaque cell autophagy.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  14. Biomedicines · 2021
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

Harald ManggeClinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, A-8036 Graz, Austria. harald.mangge@medunigraz.at.ORCID 0000-0003-4067-247X
Gunter AlmerClinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, A-8036 Graz, Austria.
Medical University of Graz · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic long-lasting vascular disease leading to myocardial infarction and stroke. Vulnerable atherosclerotic (AS) plaques are responsible for these life-threatening clinical endpoints. To more successfully work against atherosclerosis, improvements in early diagnosis and treatment of AS plaque lesions are required. Vulnerable AS plaques are frequently undetectable by conventional imaging because they are non-stenotic. Although blood biomarkers like lipids, C-reactive protein, interleukin-6, troponins, and natriuretic peptides are in pathological ranges, these markers are insufficient in detecting the critical perpetuation of AS anteceding endpoints. Thus, chances to treat the patient in a preventive way are wasted. It is now time to solve this dilemma because clear results indicate a benefit of anti-inflammatory therapy per se without modification of blood lipids (CANTOS Trial, NCT01327846). This fact identifies modulation of immune-mediated inflammation as a new promising point of action for the eradication of fatal atherosclerotic endpoints.

Indexed as

Disease SusceptibilityAdaptive ImmunityAnimalsBiomarkersHumansImmune SystemImmunity, InnateInflammationMatrix MetalloproteinasesNeovascularization, PathologicPlaque, AtheroscleroticBiomarkersMatrix Metalloproteinasesatherosclerosiscardiovascular diseaseimmune activationinflammation

Identifiers

PMID31450823
PMCPMC6749340
OpenAlexW2969263951

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.