Evidence map›Paper›PMID 31504400›Full record

ArticleEuropean heart journal2020

Clonal haematopoiesis in patients with degenerative aortic valve stenosis undergoing transcatheter aortic valve implantation.

Silvia Mas-Peiro, Jedrzej Hoffmann, Stephan Fichtlscherer, Lena Dorsheimer, Michael A Rieger, Stefanie Dimmeler, Mariuca Vasa-Nicotera, Andreas M Zeiher

Open access · hybridAbstract read
In one paragraph

Article in European heart journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 2 pooled it
17.8field-weighted citation impact, top 1% 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

149 citing papers in PubMed, 2 syntheses or guidelines pooled it, 221 citations in OpenAlex.

  1. Clonal Hematopoiesis of Indeterminate Potential and Kidney Function Decline in the General Population.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2023
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  11. Exacerbation of inflammatory bone loss in TET2-driven clonal hematopoiesis.Journal of immunology (Baltimore, Md. : 1950) · 2026
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89 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Silvia Mas-PeiroDepartment of Medicine, Cardiology, Goethe University Hospital, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
Jedrzej HoffmannDepartment of Medicine, Cardiology, Goethe University Hospital, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
Stephan FichtlschererDepartment of Medicine, Cardiology, Goethe University Hospital, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
Lena DorsheimerDepartment of Medicine, Haematology/Oncology, Goethe University Hospital, Frankfurt, Germany.
Michael A RiegerDepartment of Medicine, Haematology/Oncology, Goethe University Hospital, Frankfurt, Germany.
Stefanie DimmelerGerman Centre for Cardiovascular Research, Berlin, Partner Site Frankfurt Rhine-Main, Germany.
Mariuca Vasa-NicoteraDepartment of Medicine, Cardiology, Goethe University Hospital, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
Andreas M ZeiherDepartment of Medicine, Cardiology, Goethe University Hospital, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsClonal haematopoiesis of indeterminate potential (CHIP), defined as the presence of an expanded somatic blood cell clone without other haematological abnormalities, was recently shown to increase with age and is associated with coronary artery disease and calcification. The most commonly mutated CHIP genes, DNMT3A and TET2, were shown to regulate inflammatory potential of circulating leucocytes. The incidence of degenerative calcified aortic valve (AV) stenosis increases with age and correlates with chronic inflammation. We assessed the incidence of CHIP and its association with inflammatory blood cell phenotypes in patients with AV stenosis undergoing transfemoral aortic valve implantation (TAVI). METHODS AND

resultsTargeted amplicon sequencing for DNMT3A and TET2 was performed in 279 patients with severe AV stenosis undergoing TAVI. Somatic DNMT3A- or TET2-CHIP-driver mutations with a VAF ≥ 2% were detected in 93 out of 279 patients (33.3%), with an age-dependent increase in the incidence from 25% (55-69 years) to 52.9% (90-100 years). Patients with DNMT3A- or TET2-CHIP-driver mutations did not differ from patients without such mutations in clinical parameters, concomitant atherosclerotic disease, blood cell counts, inflammatory markers, or procedural characteristics. However, patients with DNMT3A- or TET2-CHIP-driver mutations had a profoundly increased medium-term all-cause mortality following successful TAVI. Differential myeloid and T-cell distributions revealed pro-inflammatory T-cell polarization in DNMT3A-mutation carriers and increased pro-inflammatory non-classical monocytes in TET2-mutation carriers.

conclusionThis is the first study to show that acquired somatic mutations in the most commonly mutated CHIP-driver genes occur frequently in patients with severe degenerative AV stenosis, are associated with increased pro-inflammatory leucocyte subsets, and confer a profound increase in mortality following successful TAVI.

Indexed as

Aortic Valve StenosisCalcinosisTranscatheter Aortic Valve ReplacementAgedAortic ValveClonal HematopoiesisHumansMiddle AgedRisk FactorsTreatment OutcomeAortic valve diseaseClonal haematopoiesisInflammationTAVI

Identifiers

PMID31504400
PMCPMC7033916
OpenAlexW2971653336

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.