Prevention & lipidsCohort study

Lipoprotein(a), Inflammation, and Risk of Coronary Artery Disease and Aortic Valve Stenosis

JAMA CardiolPublished

  • Prospective cohort study
  • population-based

Authors' conclusion

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.

Study context

Population
UK Biobank adults without prevalent coronary artery disease (CAD) or AS who underwent plasma proteomic profiling; primary prevention
Participants
43,512 adults
Exposure
Lp ≥125 nmol/L vs <125 nmol/L, by inflammatory biomarker levels
  • Lp(a) ≥125 nmol/Ln = 6,975
Outcome
Incident CAD
Follow-up
Median 13.5 years

Main finding

As reported in the abstract

Incident CAD, by IL-6 quartile (interaction)
Lp(a) ≥125 nmol/L vs Lp(a) <125 nmol/LHazard ratio (95% CI)
IL-6 quartile 4
1.43(1.25–1.63)
IL-6 quartile 1
1.09(0.85–1.38)

Observational data: associations, not effects.

Secondary outcomes

Incident CAD, Lp(a) × neutrophil to lymphocyte ratio (NLR) interaction

Suggestive but not significant after adjustment for multiple testing
P for interaction = 0.02

Incident AS · median follow-up 13.6 years

No inflammatory biomarkers modified Lp(a)-associated risk for AS

Original publication

Lipoprotein(a), Inflammation, and Risk of Coronary Artery Disease and Aortic Valve Stenosis. JAMA Cardiol. Published 1 August 2026. doi:10.1001/jamacardio.2026.1852

Summarised from the published abstract; every number is checked against it