Evidence map›Paper›PMID 29136138›Full record

ReviewEuropean heart journal2018

Calcific aortic valve stenosis: hard disease in the heart: A biomolecular approach towards diagnosis and treatment.

Frederique E C M Peeters, Steven J R Meex, Marc R Dweck, Elena Aikawa, Harry J G M Crijns, Leon J Schurgers, Bas L J H Kietselaer

Open access · bronzeAbstract readReview
In one paragraph

Review in European heart journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
7.0field-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

100 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.

  1. Pooled it
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  18. Dysglycaemia and incident aortic stenosis: a cohort study.Heart (British Cardiac Society) · 2025
    Article
  19. Review
  20. Article

40 more citing papers are in PubMed but not listed here.

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 3 institutions in 3 countries.

Frederique E C M PeetersDepartment of Cardiology, MUMC+ and CARIM, P. Debyelaan 25, HX Maastricht, the Netherlands.
Steven J R MeexDepartment of Clinical Chemistry, MUMC+, P. Debyelaan 25, HX Maastricht, the Netherlands.
Marc R DweckCentre for Cardiovascular Science, University of Edinburgh, 47 Little France Crescent, Edinburgh, UK.
Elena AikawaDepartment of Medicine, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA, USA.
Harry J G M CrijnsDepartment of Cardiology, MUMC+ and CARIM, P. Debyelaan 25, HX Maastricht, the Netherlands.
Leon J SchurgersDepartment of Biochemistry and CARIM, Maastricht University, PO Box 616, MD Maastricht, The Netherlands.
Bas L J H KietselaerDepartment of Cardiology, MUMC+ and CARIM, P. Debyelaan 25, HX Maastricht, the Netherlands.
Harvard University · USMaastricht University · NLUniversity of Edinburgh · GB

Funding

Shear stress, endothelial miRNAs, and AV calcificationR01HL119798 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG, YOGANATHAN, AJIT P · 2013 to 2022
$4.7M
British Heart Foundation FS/13/77/30488British Heart Foundation FS/14/78/31020NHLBI NIH HHS R01 HL119798
6 · The paper itself

Abstract

Calcific aortic valve stenosis (CAVS) is common in the ageing population and set to become an increasing economic and health burden. Once present, it inevitably progresses and has a poor prognosis in symptomatic patients. No medical therapies are proven to be effective in holding or reducing disease progression. Therefore, aortic valve replacement remains the only available treatment option. Improved knowledge of the mechanisms underlying disease progression has provided us with insights that CAVS is not a passive disease. Rather, CAVS is regulated by numerous mechanisms with a key role for calcification. Aortic valve calcification (AVC) is actively regulated involving cellular and humoral factors that may offer targets for diagnosis and intervention. The discovery that the vitamin K-dependent proteins are involved in the inhibition of AVC has boosted our mechanistic understanding of this process and has opened up novel avenues in disease exploration. This review discusses processes involved in CAVS progression, with an emphasis on recent insights into calcification, methods for imaging calcification activity, and potential therapeutic options.

Indexed as

Aortic ValveAortic Valve StenosisCalcinosisHumansMolecular Diagnostic TechniquesMolecular Targeted Therapy

Identifiers

PMID29136138
PMCPMC6055545
OpenAlexW2767302812

What OpenQuestion 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 OpenQuestion graph.