Evidence map›Paper›PMID 40892620›Full record

Trial reportJournal of the American College of Cardiology2025

Colchicine and Longitudinal Dynamics of Clonal Hematopoiesis: An Exploratory Substudy of the LoDoCo2 Trial.

Niekbachsh Mohammadnia, Liying Xue, Lucas T W Vestjens, Md Mesbah Uddin, Abhishek Niroula, Dominique P V de Kleijn, Arend Mosterd, Aernoud T L Fiolet, Tetsushi Nakao, John W Eikelboom and 8 more

Abstract readRandomized Controlled Trial
In one paragraph

Trial report in Journal of the American College of Cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Review
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  6. Genetic factors contributing to atherosclerosis.Current opinion in cardiology · 2026
    Review
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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

18 authors.

Niekbachsh MohammadniaDepartment of Cardiology, Radboud University Medical Center, Nijmegen, the Netherlands.
Liying XueBroad Institute of MIT and Harvard, Cambridge, Massachusetts, USA.
Lucas T W VestjensDepartment of Cardiology, Radboud University Medical Center, Nijmegen, the Netherlands.
Md Mesbah UddinBroad Institute of MIT and Harvard, Cambridge, Massachusetts, USA; Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts, USA.
Abhishek NiroulaBroad Institute of MIT and Harvard, Cambridge, Massachusetts, USA; Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Science for Life Laboratory, University of Gothenburg, Gothenburg, Sweden.
Dominique P V de KleijnDepartment of Vascular Surgery, University Medical Center Utrecht, Utrecht, the Netherlands.
Arend MosterdDutch Network for Cardiovascular Research (WCN), Utrecht, the Netherlands; Department of Cardiology, Meander Medical Center, Amersfoort, the Netherlands.
Aernoud T L FioletDepartment of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.
Tetsushi NakaoBroad Institute of MIT and Harvard, Cambridge, Massachusetts, USA.
John W EikelboomDepartment of Medicine, McMaster University, Hamilton, Ontario, Canada.
Aysun Cetinyurek-YavuzIQ Health, Radboud University Medical Center, Nijmegen, the Netherlands.
Gina M PelosoDepartment of Biostatistics, Boston University School of Public Health, Boston, Massachusetts, USA.
Willem A BaxDepartment of Internal Medicine, Noordwest Ziekenhuisgroep, Alkmaar, the Netherlands.
Niels P RiksenDepartment of Internal Medicine, Radboud University Medical Center, Nijmegen, the Netherlands.
Pradeep NatarajanBroad Institute of MIT and Harvard, Cambridge, Massachusetts, USA; Center for Genomic Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA; Heart and Vascular Institute, Mass General Brigham, Boston, Massachusetts, USA.
Jan H CornelDepartment of Cardiology, Radboud University Medical Center, Nijmegen, the Netherlands; Dutch Network for Cardiovascular Research (WCN), Utrecht, the Netherlands; Department of Cardiology, Noordwest Ziekenhuisgroep, Alkmaar, the Netherlands.
Saloua El MessaoudiDepartment of Cardiology, Radboud University Medical Center, Nijmegen, the Netherlands. Electronic address: Saloua.ElMessaoudi@radboudumc.nl.
Michael C HonigbergBroad Institute of MIT and Harvard, Cambridge, Massachusetts, USA; Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts, USA; Center for Genomic Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA; Heart and Vascular Institute, Mass General Brigham, Boston, Massachusetts, USA. Electronic address: mhonigberg@mgh.harvard.edu.

Funding

Effects of IL-1 beta inhibition on vascular inflammation in TET2 clonal hematopoiesisR01HL173028 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI Michael Honigberg, Mabel Toribio · 2025 to 2026
$1.7M
Using genomic modifiers to mechanistically link clonal hematopoiesis of indeterminate potential penetrance to coronary artery diseaseK99HL165024 · NHLBI · BROAD INSTITUTE, INC. · PI NAKAO, TETSUSHI · 2023 to 2024
$334k
American Heart Association-American Stroke Association 24RGRSG1275749American Heart Association-American Stroke Association 25SFRNCCKMS1443062American Heart Association-American Stroke Association 25SFRNPCKMS1463898NHLBI NIH HHS K99 HL165024NHLBI NIH HHS R01 HL173028
6 · The paper itself

Abstract

backgroundClonal hematopoiesis (CH) is an aging-related hematologic condition associated with increased risk for cardiovascular events. Larger CH clones associate more strongly with cardiovascular risk. Preclinical data indicate that inflammatory signaling drives expansion of CH clones and CH-associated cardiovascular disease. However, the effect of anti-inflammatory therapies on CH clonal dynamics in humans is unclear.

objectivesThe goal of this study was to test the association of randomization to colchicine vs placebo with CH growth in participants with chronic coronary artery disease. It also assessed the association of colchicine use with change in inflammatory biomarkers over time according to CH status.

methodsIn this exploratory substudy of the LoDoCo2 (Low-Dose Colchicine 2) trial, high-coverage targeted sequencing was used to detect CH driver mutations and to quantify variant allele frequency at 4 timepoints: baseline, after a 30-day open-label colchicine run-in phase (0.5 mg daily), 1 year postrandomization to colchicine or placebo, and at end of study (median follow-up of 25.0 months). Clonal dynamics were assessed by using a generalized linear mixed model. High-sensitivity C-reactive protein and interleukin-6 were additionally measured at baseline, randomization, and 1 year postrandomization.

resultsIn total, 854 participants contributed 2,047 observations across 4 timepoints, including before and after the prerandomization colchicine run-in period. Randomization to placebo was associated with a 14.9% annual increase in CH clone size (β

conclusionsIn this exploratory analysis, treatment with low-dose colchicine was associated with attenuated clonal expansion in TET2 CH. These findings suggest the potential for colchicine to curb the proliferative advantage of key CH driver mutations and to mitigate their associated risk of cardiovascular disease. Further validation in prospective studies is warranted.

Indexed as

Clonal HematopoiesisColchicineCoronary Artery DiseaseAgedFemaleHumansInterleukin-6Longitudinal StudiesMaleMiddle AgedColchicineInterleukin-6clonal dynamicsclonal hematopoiesiscolchicinehsCRPIL-6inflammation

Identifiers

PMID40892620
PMCPMC12557339

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.