Evidence map›Paper›PMID 37475157›Full record

ArticleCardiovascular research2023

A machine learning based approach to identify carotid subclinical atherosclerosis endotypes.

Qiao Sen Chen, Otto Bergman, Louise Ziegler, Damiano Baldassarre, Fabrizio Veglia, Elena Tremoli, Rona J Strawbridge, Antonio Gallo, Matteo Pirro, Andries J Smit and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

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  7. Interpretable machine learning analysis for relationships betweenFrontiers in cellular and infection microbiology · 2026
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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

15 authors at 9 institutions in 6 countries.

Qiao Sen ChenDivision of Cardiovascular Medicine, Department of Medicine Solna, Karolinska Institutet, Solnavägen 30, 171 64 Stockholm, Sweden.ORCID 0000-0002-5864-7574
Otto BergmanDivision of Cardiovascular Medicine, Department of Medicine Solna, Karolinska Institutet, Solnavägen 30, 171 64 Stockholm, Sweden.
Louise ZieglerDivision of Medicine and Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Entrevägen 2, 182 88 Stockholm, Sweden.
Damiano BaldassarreDepartment of Medical Biotechnology and Translational Medicine, Università di Milano, Via Vanvitelli 32, 20133 Milan, Italy.ORCID 0000-0002-2766-8882
Fabrizio VegliaMaria Cecilia Hospital, GVM Care & Research, Via Corriera 1, 48033 Cotignola (RA), Italy.
Elena TremoliMaria Cecilia Hospital, GVM Care & Research, Via Corriera 1, 48033 Cotignola (RA), Italy.
Rona J StrawbridgeDivision of Cardiovascular Medicine, Department of Medicine Solna, Karolinska Institutet, Solnavägen 30, 171 64 Stockholm, Sweden.
Antonio GalloLipidology and Cardiovascular Prevention Unit, Department of Nutrition, Sorbonne Université, INSERM UMR1166, APHP, Hôpital Pitié-Salpètriêre, 47 Boulevard de l´Hopital, 75013 Paris, France.
Matteo PirroInternal Medicine, Angiology and Arteriosclerosis Diseases, Department of Medicine, University of Perugia, Piazzale Menghini 1, 06129 Perugia, Italy.
Andries J SmitDepartment of Medicine, University Medical Center Groningen, Groningen & Isala Clinics Zwolle, Dokter Spanjaardweg 29B, 8025 BT Groningen, the Netherlands.
Sudhir KurlInstitute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio Campus, Yliopistonranta 1 C, Canthia Building, B Wing, FI-70211 Kuopio, Finland.
Kai SavonenKuopio Research Institute of Exercise Medicine, Haapaniementie 16, FI-70100 Kuopio, Finland.
Lars LindDepartment of Medical Sciences, Uppsala University, Uppsala Science Park, Dag Hammarskjöldsv 10B, 752 37 Uppsala, Sweden.ORCID 0000-0003-2335-8542
Per ErikssonDivision of Cardiovascular Medicine, Department of Medicine Solna, Karolinska Institutet, Solnavägen 30, 171 64 Stockholm, Sweden.
Bruna GiganteDivision of Cardiovascular Medicine, Department of Medicine Solna, Karolinska Institutet, Solnavägen 30, 171 64 Stockholm, Sweden.ORCID 0000-0003-4508-7990
Karolinska Institutet · SEMaria Cecilia Hospital · ITUniversity of Eastern Finland · FIDanderyds sjukhus · SEInserm · FRUniversity Medical Center Groningen · NLUniversity of Milan · ITUniversity of Perugia · ITUppsala University · SE

Funding

Stiftelsen Professor Nanna Svartz fondStiftelsen Sigurd & Elsa Goljes minne
6 · The paper itself

Abstract

aimsTo define endotypes of carotid subclinical atherosclerosis. METHODS AND

resultsWe integrated demographic, clinical, and molecular data (n = 124) with ultrasonographic carotid measurements from study participants in the IMPROVE cohort (n = 3340). We applied a neural network algorithm and hierarchical clustering to identify carotid atherosclerosis endotypes. A measure of carotid subclinical atherosclerosis, the c-IMTmean-max, was used to extract atherosclerosis-related features and SHapley Additive exPlanations (SHAP) to reveal endotypes. The association of endotypes with carotid ultrasonographic measurements at baseline, after 30 months, and with the 3-year atherosclerotic cardiovascular disease (ASCVD) risk was estimated by linear (β, SE) and Cox [hazard ratio (HR), 95% confidence interval (CI)] regression models. Crude estimates were adjusted by common cardiovascular risk factors, and baseline ultrasonographic measures. Improvement in ASCVD risk prediction was evaluated by C-statistic and by net reclassification improvement with reference to SCORE2, c-IMTmean-max, and presence of carotid plaques. An ensemble stacking model was used to predict endotypes in an independent validation cohort, the PIVUS (n = 1061). We identified four endotypes able to differentiate carotid atherosclerosis risk profiles from mild (endotype 1) to severe (endotype 4). SHAP identified endotype-shared variables (age, biological sex, and systolic blood pressure) and endotype-specific biomarkers. In the IMPROVE, as compared to endotype 1, endotype 4 associated with the thickest c-IMT at baseline (β, SE) 0.36 (0.014), the highest number of plaques 1.65 (0.075), the fastest c-IMT progression 0.06 (0.013), and the highest ASCVD risk (HR, 95% CI) (1.95, 1.18-3.23). Baseline and progression measures of carotid subclinical atherosclerosis and ASCVD risk were associated with the predicted endotypes in the PIVUS. Endotypes consistently improved measures of ASCVD risk discrimination and reclassification in both study populations.

conclusionsWe report four replicable subclinical carotid atherosclerosis-endotypes associated with progression of atherosclerosis and ASCVD risk in two independent populations. Our approach based on endotypes can be applied for precision medicine in ASCVD prevention.

Indexed as

AtherosclerosisCardiovascular DiseasesCarotid Artery DiseasesPlaque, AtheroscleroticCarotid ArteriesHumansRisk FactorsArtificial intelligenceASCVDAtherosclerosisBiological markersEndotypeProgression of atherosclerosis

Identifiers

PMID37475157
PMCPMC10730242
OpenAlexW4384926275

What OpenQuestion holds

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LicenceCC BY
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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.