Evidence map›Paper›PMID 35743402›Full record

ReviewJournal of clinical medicine2022

Implication of Lipids in Calcified Aortic Valve Pathogenesis: Why Did Statins Fail?

Mohamed J Nsaibia, Anichavezhi Devendran, Eshak Goubaa, Jamal Bouitbir, Romain Capoulade, Rihab Bouchareb

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  14. Review
  15. Review
  16. Lipoprotein(a): Emerging insights and therapeutics.American journal of preventive cardiology · 2024
    Article
  17. Review
  18. 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

6 authors at 5 institutions in 3 countries.

Mohamed J NsaibiaDepartment of Cell Biology and Molecular Medicine, Rutgers University, Newark, NJ 07103, USA.
Anichavezhi DevendranDepartment of Medicine, Cardiovascular Research Institute, The Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.ORCID 0000-0002-2483-7660
Eshak GoubaaThomas Jefferson University East Falls, Philadelphia, PA 19144, USA.
Jamal BouitbirDepartment of Pharmaceutical Sciences, Division of Molecular and Systems Toxicology, University of Basel, 4056 Basel, Switzerland.ORCID 0000-0003-4453-9457
Romain CapouladeL'institut Du Thorax, Nantes Université, CNRS, INSERM, F-44000 Nantes, France.ORCID 0000-0002-7233-7409
Rihab BoucharebDepartment of Medicine, Division of Nephrology, The Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.ORCID 0000-0002-6468-1269
Icahn School of Medicine at Mount Sinai · USCentre National de la Recherche Scientifique · FRRutgers, The State University of New Jersey · USThomas Jefferson University · USUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcific Aortic Valve Disease (CAVD) is a fibrocalcific disease. Lipoproteins and oxidized phospholipids play a substantial role in CAVD; the level of Lp(a) has been shown to accelerate the progression of valve calcification. Indeed, oxidized phospholipids carried by Lp(a) into the aortic valve stimulate endothelial dysfunction and promote inflammation. Inflammation and growth factors actively promote the synthesis of the extracellular matrix (ECM) and trigger an osteogenic program. The accumulation of ECM proteins promotes lipid adhesion to valve tissue, which could initiate the osteogenic program in interstitial valve cells. Statin treatment has been shown to have the ability to diminish the death rate in subjects with atherosclerotic impediments by decreasing the serum LDL cholesterol levels. However, the use of HMG-CoA inhibitors (statins) as cholesterol-lowering therapy did not significantly reduce the progression or the severity of aortic valve calcification. However, new clinical trials targeting Lp(a) or PCSK9 are showing promising results in reducing the severity of aortic stenosis. In this review, we discuss the implication of lipids in aortic valve calcification and the current findings on the effect of lipid-lowering therapy in aortic stenosis.

Indexed as

aortic valvelipidsLp(a)PCSK9statins

Identifiers

PMID35743402
PMCPMC9225514
OpenAlexW4281786641

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.