Evidence map›Paper›PMID 32477143›Full record

ReviewFrontiers in pharmacology2020

Calcific Aortic Valve Disease-Natural History and Future Therapeutic Strategies.

Brunilda Alushi, Lavinia Curini, Mary Roxana Christopher, Herko Grubitzch, Ulf Landmesser, Amedeo Amedei, Alexander Lauten

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Lipoprotein(a) and panvascular disease.Lipids in health and disease · 2025
    Review
  12. Age Differences in Aortic Stenosis.Reviews in cardiovascular medicine · 2025
    Review
  13. [The association between biological aging markers and valvular heart diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Article
  14. Review
  15. Iranian journal of public health · 2024
    Article
  16. Review
  17. Review
  18. CircRNAJournal of thoracic disease · 2023
    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

7 authors at 5 institutions in 2 countries.

Brunilda AlushiDepartment of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.
Lavinia CuriniDepartment of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.
Mary Roxana ChristopherDepartment of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.
Herko GrubitzchBerlin Institute of Health, Berlin, Germany.
Ulf LandmesserDepartment of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.
Amedeo AmedeiDepartment of Experimental and Clinical Medicine, University of Florence, Firenze, Italy.
Alexander LautenDepartment of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.
Charité - Universitätsmedizin Berlin · DEGerman Centre for Cardiovascular Research · DEAzienda Ospedaliero-Universitaria Careggi · ITBerlin Institute of Health at Charité - Universitätsmedizin Berlin · DEHelios Klinikum Erfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcific aortic valve disease (CAVD) is the most frequent heart valve disorder. It is characterized by an active remodeling process accompanied with valve mineralization, that results in a progressive aortic valve narrowing, significant restriction of the valvular area, and impairment of blood flow.The pathophysiology of CAVD is a multifaceted process, involving genetic factors, chronic inflammation, lipid deposition, and valve mineralization. Mineralization is strictly related to the inflammatory process in which both, innate, and adaptive immunity are involved. The underlying pathophysiological pathways that go from inflammation to calcification and, finally lead to severe stenosis, remain, however, incompletely understood. Histopathological studies are limited to patients with severe CAVD and no samples are available for longitudinal studies of disease progression. Therefore, alternative routes should be explored to investigate the pathogenesis and progression of CAVD.Recently, increasing evidence suggests that epigenetic markers such as non-coding RNAs are implicated in the landscape of phenotypical changes occurring in CAVD. Furthermore, the microbiome, an essential player in several diseases, including the cardiovascular ones, has recently been linked to the inflammation process occurring in CAVD. In the present review, we analyze and discuss the CAVD pathophysiology and future therapeutic strategies, focusing on the real and putative role of inflammation, calcification, and microbiome.

Indexed as

aortic valve replacementcalcific aortic valveimmune systeminflammationmicrobiomesevere aortic stenosisTAVR

Identifiers

PMID32477143
PMCPMC7237871
OpenAlexW3026014143

What Socratic 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 Socratic graph.