Evidence map›Paper›PMID 40567226›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2025

Human Genetic Evidence Does Not Support a Causal Role for Reduced FXI Levels in Heart Failure Pathogenesis-Brief Report.

Iyas Daghlas, Dipender Gill

Abstract read
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Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Factor XI and Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Iyas DaghlasDepartment of Neurology, University of California San Francisco Weill Institute for Neurosciences, University of California San Francisco (I.D.).ORCID 0000-0001-6924-0641
Dipender GillDepartment of Epidemiology and Biostatistics, School of Public Health, Imperial College London, United Kingdom (D.G.).ORCID 0000-0001-7312-7078

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCoagulation factor XI (FXI) is a promising therapeutic target for preventing thromboembolic disease while preserving hemostasis. However, recent translational and epidemiological findings have raised concerns that lowering FXI levels may increase heart failure risk. To clarify these potential risks, we investigated whether lifelong genetically reduced FXI levels were associated with risk of heart failure and imaging correlates of cardiovascular function.

methodsWe used a genome-wide association study of circulating FXI levels in the deCODE cohort (N=35 559) to identify a genetic proxy in the

resultsWe identified an

conclusionsCurrent human genetic evidence does not support an adverse effect of lower FXI levels on heart failure risk or cardiovascular function. Further studies examining the effect of FXI levels on cardiac events and function are warranted.

Indexed as

Factor XIHeart FailureAgedCase-Control StudiesFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMaleMendelian Randomization AnalysisMiddle AgedPhenotypePolymorphism, Single NucleotideRisk AssessmentRisk FactorsFactor XIatrial fibrillationfactor XIgenome-wide association studyheart failuremagnetic resonance imaging

Identifiers

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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.