Evidence map›Paper›PMID 32492156›Full record

ArticleBlood advances2020

High-sensitivity C-reactive protein is associated with clonal hematopoiesis of indeterminate potential.

Lambert Busque, Maxine Sun, Manuel Buscarlet, Sami Ayachi, Yassamin Feroz Zada, Sylvie Provost, Vincent Bourgoin, Luigina Mollica, Marlies Meisel, Reinhard Hinterleitner and 3 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.5field-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

52 citing papers in PubMed, 94 citations in OpenAlex.

  1. Trial
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  4. Clonal hematopoiesis and thrombosis risk-what are research and clinical gaps?Research and practice in thrombosis and haemostasis · 2026
    Review
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  8. Article
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  12. Clonal Hematopoiesis and Thrombosis.American journal of hematology · 2025
    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

13 authors at 5 institutions in 2 countries.

Lambert BusqueResearch Center.
Maxine SunDepartment of Medicine, Université de Montréal, Montreal, Canada.
Manuel BuscarletResearch Center.
Sami AyachiResearch Center.
Yassamin Feroz ZadaBeaulieu-Saucier Pharmacogenomics Center, Montreal Heart Institute, Montreal, Canada.
Sylvie ProvostBeaulieu-Saucier Pharmacogenomics Center, Montreal Heart Institute, Montreal, Canada.
Vincent BourgoinResearch Center.
Luigina MollicaResearch Center.
Marlies MeiselDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA; and.
Reinhard HinterleitnerDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA; and.
Bana JabriDepartment of Medicine, University of Chicago, Chicago, IL.
Marie-Pierre DubéDepartment of Medicine, Université de Montréal, Montreal, Canada.
Jean-Claude TardifDepartment of Medicine, Université de Montréal, Montreal, Canada.
Montreal Heart Institute · CAHôpital Maisonneuve-Rosemont · CAUniversity of Pittsburgh · USUniversité de Montréal · CAUniversity of Chicago · US

Funding

CIHR
6 · The paper itself

Abstract

Clonal hematopoiesis of indeterminate potential (CHIP) is predictive of hematological cancers and cardiovascular diseases, but the etiology of CHIP initiation and clonal expansion is unknown. Several lines of evidence suggest that proinflammatory cytokines may favor mutated hematopoietic stem cell expansion. To investigate the potential link between inflammation and CHIP, we performed targeted deep sequencing of 11 genes previously implicated in CHIP in 1887 subjects aged >70 years from the Montreal Heart Institute Biobank, of which 1359 had prior coronary artery disease (CAD), and 528 controls did not. We assessed association of CHIP with log transformed high-sensitivity C-reactive protein (hs-CRP), a validated biomarker of inflammation. CHIP was identified in 427 of the 1887 subjects (22.6%). CHIP mutations were more frequently identified in DNMT3A (11.6%) and TET2 (6.1%), with a higher proportion of TET2 mutations occurring in controls than in patients with CAD (9.0% vs 4.9%, P < .001). CHIP carriers had 21% higher hs-CRP levels compared with their noncarrier counterparts (eβ = 1.21, 95% confidence interval [CI]: 1.08 to 1.36; P = .001). A similar effect was observed in the subgroup of patients with known CAD (eβ = 1.22, 95% CI: 1.06 to 1.41; P = .005). These findings confirm the association between inflammation and CHIP. This association may open investigational avenues aimed at documenting mechanisms linking inflammation to clonal progression and ultimately supports prevention interventions to attenuate CHIP's impact on cardiovascular disease and cancer.

Indexed as

Clonal HematopoiesisC-Reactive ProteinHematopoiesisPercutaneous Coronary InterventionAgedAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsHematopoietic Stem CellsHumansMaleAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsC-Reactive Protein

Identifiers

PMID32492156
PMCPMC7284088
OpenAlexW3032758825

What OpenQuestion holds

Textmetadata
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.