Evidence map›Paper›PMID 30344956›Full record

ReviewWorld journal of cardiology2018

Established and novel pathophysiological mechanisms of pericardial injury and constrictive pericarditis.

Vinasha Ramasamy, Bongani M Mayosi, Edward D Sturrock, Mpiko Ntsekhe

Abstract readReview
In one paragraph

Review in World journal of cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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.

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

21 citing papers in PubMed.

  1. Review
  2. Article
  3. Zinc: a metallic shield against cardiac inflammation.Metallomics : integrated biometal science · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Pericarditis caused by Proteus mirabilis in sheep.Veterinary medicine and science · 2023
    Article
  10. Effusive-constrictive pericarditis as first manifestation of late-onset systemic lupus erythematosus: an atypical case with grave prognosis.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2023
    Article
  11. A case report: symptomatic pericarditis post-COVID-19 vaccination.European heart journal. Case reports · 2021
    Article
  12. Pericardiectomy for constrictive pericarditis in a resource constraint setting.Kardiochirurgia i torakochirurgia polska = Polish journal of cardio-thoracic surgery · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cardiac Immunology: A New Era for Immune Cells in the Heart.Advances in experimental medicine and biology · 2021
    Review
  18. Article
  19. Article
  20. Review
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.

Vinasha RamasamyInstitute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa.
Bongani M MayosiInstitute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa.
Edward D SturrockInstitute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa.
Mpiko NtsekheInstitute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review article aims to: (1) discern from the literature the immune and inflammatory processes occurring in the pericardium following injury; and (2) to delve into the molecular mechanisms which may play a role in the progression to constrictive pericarditis. Pericarditis arises as a result of a wide spectrum of pathologies of both infectious and non-infectious aetiology, which lead to various degrees of fibrogenesis. Current understanding of the sequence of molecular events leading to pathological manifestations of constrictive pericarditis is poor. The identification of key mechanisms and pathways common to most fibrotic events in the pericardium can aid in the design and development of novel interventions for the prevention and management of constriction. We have identified through this review various cellular events and signalling cascades which are likely to contribute to the pathological fibrotic phenotype. An initial classical pattern of inflammation arises as a result of insult to the pericardium and can exacerbate into an exaggerated or prolonged inflammatory state. Whilst the implication of major drivers of inflammation and fibrosis such as tumour necrosis factor and transforming growth factor β were foreseeable, the identification of pericardial deregulation of other mediators (basic fibroblast growth factor, galectin-3 and the tetrapeptide Ac-SDKP) provides important avenues for further research.

Indexed as

Autoimmune diseaseConstrictive pericarditisFibrosis mechanismInflammatory pericarditisTuberculous pericarditis

Identifiers

PMID30344956
PMCPMC6189073

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Registered trials

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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.