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.
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).
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%) had Lp(a) levels of 125 nmol/L or higher, 24,079 (55%) were female, and overall mean age was 56 years.
Median follow-up was 13 years for incident CAD and 14 years for incident AS.
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 (40-60% higher).
No inflammatory biomarkers modified Lp(a)-associated risk for AS.
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. These findings identify IL-6 as a biomarker of inflammatory risk that may modify Lp(a)-associated CAD risk.
At the KAHN CENTER, we have been checking levels of IL-6 in most patients and all of those with an elevated Lp(a). We need better tools to predict who is truly at high risk carrying high levels of Lp(a), and this available blood test is an important advance.
