Evidence map›Paper›PMID 41107060›Full record

ArticleOpen heart2025

Causal relevance of clonal haematopoiesis with cardiac disease and adverse remodelling: a Mendelian randomisation study.

Alec Peter Morley, Maddalena Ardissino, Paul Carter, Betty Raman, Adam J Mead, Pedro M Quiros, George S Vassiliou, Zahra Raisi-Estabragh

Abstract read
In one paragraph

Article in Open heart, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
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

8 authors.

Alec Peter MorleyGonville and Caius College, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0009-0005-6021-2093
Maddalena ArdissinoBritish Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK.
Paul CarterVictor Phillip Dahdaleh Heart and Lung Research Institute, University of Cambridge, Cambridge, UK.
Betty RamanDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, National Institute for Health Research Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.
Adam J MeadMedical Research Council (MRC) Weatherall Institute of Molecular Medicine (WIMM) and NIHR Biomedical Research Centre, University of Oxford, Oxford, UK.
Pedro M QuirosDepartment of Biochemistry and Molecular Biology, Instituto Universitario de Oncología (IUOPA), Universidad de Oviedo, Oviedo, Spain.
George S VassiliouCambridge Stem Cell Institute, University of Cambridge, Cambridge, UK.
Zahra Raisi-EstabraghWilliam Harvey Research Institute, NIHR Barts Biomedical Research Centre, Queen Mary University of London, London, UK z.r.raisi-estabragh@qmul.ac.uk.ORCID http://orcid.org/0000-0002-7757-5465

Funding

Wellcome Trust
6 · The paper itself

Abstract

backgroundMany observational studies highlight clonal haematopoiesis (CH) as a novel determinant of cardiovascular disease (CVD). However, disentangling cause and effect from important confounders, such as age and smoking, is challenging.

objectivesMendelian randomisation (MR) was used to assess the causal relationships of CH with (1) major CVD outcomes associated with adverse remodelling, and (2) cardiovascular magnetic resonance (CMR) phenotypes which have not been examined previously.

methodsUncorrelated (r

resultsBoth

conclusionsCommon forms of CH are associated with higher AF risk and adverse remodelling patterns comprising larger atrial and ventricular sizes, myocardial fibrosis, and reduced aortic compliance. Using MR methods, this study triangulates previous observational studies and provides new evidence to support likely causal links between CH and CVD. This study, for the first time, describes associations of CH with adverse CMR phenotypes suggesting early remodelling patterns; these changes may indicate a window of opportunity for intervention such as by risk stratification and early preventative strategies to improve patient outcomes; however, further examination of the utility of such interventions is warranted.

Indexed as

Clonal HematopoiesisHeart DiseasesMendelian Randomization AnalysisPolymorphism, Single NucleotideVentricular RemodelingDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3AFemaleGenome-Wide Association StudyHumansMagnetic Resonance Imaging, CineMalePhenotypeRisk AssessmentDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanTET2 protein, humanGeneticsHeart FailureMagnetic Resonance ImagingRisk Factors

Identifiers

PMID41107060
PMCPMC12542733

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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.