ArticleJAMA cardiology2026
Lipoprotein(a), Inflammation, and Risk of Coronary Artery Disease and Aortic Valve Stenosis.
Article in JAMA 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.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Importance: Clinical heterogeneity exists among individuals with elevated lipoprotein(a) [Lp(a)] levels. Prior studies suggest that low-grade inflammation may modify this risk, but results remain conflicting. Objective: To test the hypothesis that inflammatory biomarkers may modify Lp(a)-associated risk for coronary artery disease (CAD) and aortic valve stenosis (AS) in a primary prevention population. Design, Setting, and Participants: Recruitment occurred between March 2006 through October 2010 among a population-based cohort of UK adults. UK Biobank participants without prevalent CAD or AS who underwent plasma proteomic profiling at study entry were eligible for inclusion. Data were analyzed from June 2025 through April 2026. Exposures: Lp(a) levels (<125 nmol/L vs ≥125 nmol/L) and inflammatory biomarkers interleukin 1β (IL-1β), IL-18, IL-6, and the neutrophil to lymphocyte ratio (NLR). Main Outcomes and Measures: The primary outcome was the risk of incident CAD. The secondary outcome was the risk of incident AS. Results: Among 43 512 UK Biobank participants, 6975 (16.0%) had Lp(a) levels of 125 nmol/L or higher, 24 079 (55.3%) were female, and overall mean (SD) age was 56.5 (8.2) years. Median (Q1-Q3) follow-up was 13.5 (12.7-14.3) years for incident CAD and 13.6 (12.9-14.4) years for incident AS. Multivariable-adjusted Cox proportional hazards models tested the interaction between Lp(a) levels and each inflammatory biomarker in relation to the primary and secondary outcomes. Among inflammatory biomarkers tested, IL-6 demonstrated the strongest association with both incident CAD and AS. IL-6 levels modified Lp(a)-associated risk for incident CAD (hazard ratio [HR] for Lp(a) ≥125 nmol/L vs <125 nmol/L in quartile 4 of IL-6: 1.43; 95% CI, 1.25-1.63 vs in quartile 1 of IL-6: HR, 1.09; 95% CI, 0.85-1.38; P for interaction = .008). The interaction between Lp(a) and the NLR (P for interaction = .02) was suggestive but not significant after adjustment for multiple testing. No inflammatory biomarkers modified Lp(a)-associated risk for AS. Conclusions and Relevance: In this primary prevention cohort study, Lp(a)-associated risk for incident CAD was modified by IL-6, with lower associated risk observed in the setting of lower inflammatory biomarker levels. These findings identify IL-6 as a biomarker of inflammatory risk that may modify Lp(a)-associated CAD risk.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.