Evidence map›Paper›PMID 42827879›Full record

ArticleAmerican journal of preventive cardiology2026

Multidomain risk profiles and documented polyvascular involvement across atherosclerotic vascular beds.

Kelvin Supriami, Alyssa M Flores, Yang Sui, So Mi Jemma Cho, Aniruddh P Patel, Yunfeng Ruan, Krishna G Aragam, Pradeep Natarajan, Patrick T Ellinor, Akl C Fahed

Abstract read
In one paragraph

Article in American journal of preventive cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Kelvin SupriamiDivision of Cardiology, Heart and Vascular Institute, Mass General Brigham, Boston, MA, USA.
Alyssa M FloresCardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Yang SuiDivision of Cardiology, Heart and Vascular Institute, Mass General Brigham, Boston, MA, USA.
So Mi Jemma ChoDivision of Cardiology, Heart and Vascular Institute, Mass General Brigham, Boston, MA, USA.
Aniruddh P PatelDivision of Cardiology, Heart and Vascular Institute, Mass General Brigham, Boston, MA, USA.
Yunfeng RuanDivision of Cardiology, Heart and Vascular Institute, Mass General Brigham, Boston, MA, USA.
Krishna G AragamDivision of Cardiology, Heart and Vascular Institute, Mass General Brigham, Boston, MA, USA.
Pradeep NatarajanDivision of Cardiology, Heart and Vascular Institute, Mass General Brigham, Boston, MA, USA.
Patrick T EllinorDivision of Cardiology, Heart and Vascular Institute, Mass General Brigham, Boston, MA, USA.
Akl C FahedDivision of Cardiology, Heart and Vascular Institute, Mass General Brigham, Boston, MA, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Atherosclerotic cardiovascular disease (ASCVD) manifests heterogeneously across coronary (CAD), cerebrovascular (CeVD), and peripheral artery (PAD) beds. Objectives: To evaluate sociodemographic, clinical, lifestyle, and genetic determinants of incident ASCVD, vascular bed localization, and subsequent documented polyvascular involvement. Methods: We analyzed 468,266 UK Biobank participants free of ASCVD at baseline. Risk factor associations were examined using multivariable Cox models, machine learning-derived SHapley Additive Explanations (SHAP), multinomial logistic regression, and discrete-time multistate models of clinically documented ASCVD states. Results: Among participants (mean age 57 years, 56% female) followed for 13 years, 2.8% developed CAD, 1.9% CeVD, and 1.5% PAD. Risk domains showed distinct relative associations across vascular beds. PAD onset was most strongly associated with inflammation, metabolic dysfunction, and smoking, including hsCRP (HR per SD 1.22, 95% CI 1.19-1.26); CAD was more strongly associated with LDL-C (HR 1.24, 95% CI 1.21-1.26) and CAD polygenic risk score (PRS). CeVD showed overlapping features, with additional contribution from socioeconomic deprivation. Healthy sleep and physical activity were protective across outcomes. SHAP analyses yielded similar profiles. In multinomial models, inflammation, glycemic status, and smoking were enriched in non-CAD phenotypes, whereas LDL-C and CAD PRS were more specific to CAD. PAD was most frequently followed by subsequent documented polyvascular ASCVD and mortality. In multistate models, PRSs were primarily associated with early transitions from healthy to incident ASCVD or death, whereas later documented transitions and mortality after ASCVD were more strongly linked to clinical and lifestyle factors. Conclusions: ASCVD shows distinct risk profiles across vascular beds and disease stages. Genetic factors were more strongly associated with early incident ASCVD, while clinical and lifestyle factors predominated in subsequent documented polyvascular involvement and later mortality.

Indexed as

AtherosclerosisCerebrovascular diseaseCoronary artery diseaseDisease progressionPeripheral artery diseaseRisk factors

Identifiers

PMID42827879
PMCPMC13632080

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.