Evidence map›Paper›PMID 31039577›Full record

ReviewCerebrovascular diseases extra2019

Nonsteroidal Anti-Inflammatory Drugs: A Potential Pharmacological Treatment for Intracranial Aneurysm.

Courtney L Fisher, Stacie L Demel

Open access · goldAbstract readReview
In one paragraph

Review in Cerebrovascular diseases extra, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 3 pooled it
2.8field-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.

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

19 citing papers in PubMed, 3 syntheses or guidelines pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. The effect of aspirin on aneurysm wall enhancement: A study in rabbits and humans.Interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Biophysical targeting of high-risk cerebral aneurysms.Bioengineering & translational medicine · 2022
    Article
  10. Review
  11. Repeated Aneurysm Intervention.Advances and technical standards in neurosurgery · 2022
    Article
  12. Intracranial Aneurysms Induced byFrontiers in neurology · 2022
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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.

Courtney L FisherDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan, USA, cofisher@mcw.edu.
Stacie L DemelDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan, USA.
Michigan State University · US

Funding

Cerebrovascular Fellowship Training ProgramT32NS047996 · NINDS · UNIVERSITY OF CINCINNATI · PI Joseph Paul Broderick, Stacie Demel · 2006 to 2026
$3.7M
NINDS NIH HHS T32 NS047996
6 · The paper itself

Abstract

backgroundSaccular intracranial aneurysms (IAs) are outpouchings of the vessel wall of intracranial arteries. Rupture of IAs results in subarachnoid hemorrhage which is associated with high morbidity and mortality. Surgical interventions, such as clipping and coiling, have associated risks. Currently, there are no proven pharmacological treatments to prevent the growth or rupture of IAs. Infiltration of proinflammatory cytokines in response to increased wall sheer stress is a hallmark of IA. Nonsteroidal anti-inflammatory drugs (NSAIDs) are being investigated as potential therapeutic agents for reduction in growth and/or prevention of IA through inhibition of inflammatory pathways. SUMMARY: This review will discuss the role of NSAIDs in attenuating the inflammation that drives IA progression and rupture. There are two main subtypes of NSAIDs, nonselective COX and selective COX-2 inhibitors, both of which have merit in treating IA. Evidence will be presented which shows that NSAIDs inhibit several key inflammatory mediators involved in IA progression including nuclear factor-κB, tumor necrosis factor-α, and matrix metalloproteinases. In addition, the role of NSAIDs in limiting inflammatory cell adhesion to endothelial cells and attenuating endothelial cell senescence will be discussed. Key Messages: There is an abundance of basic science and preclinical data that support NSAIDs as a promising treatment for IA. Additionally, a combination treatment strategy of low-dose aspirin given concomitantly with a selective COX-2 inhibitor may result in a reduced side effect profile compared to aspirin or selective COX-2 inhibitor use alone. Several large clinical trials are currently planned to further investigate the efficacy of NSAIDs as an effective nonsurgical treatment for IAs.

Indexed as

AnimalsAspirinCerebral ArteriesCyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsDilatation, PathologicDrug Therapy, CombinationHumansInflammation MediatorsIntracranial AneurysmSignal TransductionTreatment OutcomeVascular RemodelingAspirinCyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsInflammation MediatorsAneurysmAspirinCyclooxygenaseInflammationNonsteroidal anti-inflammatory drugs

Identifiers

PMID31039577
PMCPMC7036563
OpenAlexW2943651281

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.