Evidence map›Paper›PMID 37834945›Full record

ReviewJournal of clinical medicine2023

Influence of Aortic Valve Stenosis and Wall Shear Stress on Platelets Function.

Paweł Bańka, Maciej Wybraniec, Tomasz Bochenek, Bartosz Gruchlik, Aleksandra Burchacka, Andrzej Swinarew, Katarzyna Mizia-Stec

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.4field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Novel Circulating Biomarkers in Aortic Valve Stenosis.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. 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

7 authors at 2 institutions in 1 country.

Paweł BańkaFirst Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, 40-635 Katowice, Poland.
Maciej WybraniecFirst Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, 40-635 Katowice, Poland.ORCID 0000-0003-1151-8385
Tomasz BochenekFirst Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, 40-635 Katowice, Poland.ORCID 0000-0002-1065-2665
Bartosz GruchlikFirst Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, 40-635 Katowice, Poland.
Aleksandra BurchackaFirst Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, 40-635 Katowice, Poland.
Andrzej SwinarewFaculty of Science and Technology, University of Silesia in Katowice, 40-007 Katowice, Poland.ORCID 0000-0001-6116-9510
Katarzyna Mizia-StecFirst Department of Cardiology, School of Medicine in Katowice, Medical University of Silesia, 40-635 Katowice, Poland.ORCID 0000-0001-6907-2799
Medical University of Silesia · PLAkademii Wychowania Fizycznego im. Jerzego Kukuczki w Katowicach · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aortic valve stenosis (AS) is a common heart valve disease in the elderly population, and its pathogenesis remains an interesting area of research. The degeneration of the aortic valve leaflets gradually progresses to valve sclerosis. The advanced phase is marked by the presence of extracellular fibrosis and calcification. Turbulent, accelerated blood flow generated by the stenotic valve causes excessive damage to the aortic wall. Elevated shear stress due to AS leads to the degradation of high-molecular weight multimers of von Willebrand factor, which may involve bleeding in the mucosal tissues. Conversely, elevated shear stress has been associated with the release of thrombin and the activation of platelets, even in individuals with acquired von Willebrand syndrome. Moreover, turbulent blood flow in the aorta may activate the endothelium and promote platelet adhesion and activation on the aortic valve surface. Platelets release a wide range of mediators, including lysophosphatidic acid, which have pro-osteogenic effects in AS. All of these interactions result in blood coagulation, fibrinolysis, and the hemostatic process. This review summarizes the current knowledge on high shear stress-induced hemostatic disorders, the influence of AS on platelets and antiplatelet therapy.

Indexed as

antiplatelet therapyaortic stenosiscerebrovascular eventshemodynamicsplatelets functionvalvular heart diseasewall shear stress

Identifiers

PMID37834945
PMCPMC10573628
OpenAlexW4387168742

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.