Inflammation
High IL-6, not hsCRP, amplifies the cardiovascular mortality risk of markedly elevated Lp(a), LURIC study of 3,316 angiography patients finds (Clin Res Cardiol 2025)
Original title: Inflammation, Lp(a) and cardiovascular mortality: results from the LURIC study
This analysis of the Ludwigshafen Risk and Cardiovascular Health (LURIC) study examined 3,316 patients undergoing coronary angiography (mean age 62.6 years, predominantly male), stratified by Lp(a) (below 50 mg/dL, n = 2,668; 50-100, n = 482; above 100, n = 163), hsCRP, and IL-6, to test whether systemic inflammation modifies Lp(a)'s association with cardiovascular mortality. Lp(a) above 100 mg/dL was associated with higher cardiovascular mortality versus below 50 mg/dL (HR 1.5, 95% CI 1.06-2.12), as were hsCRP above 2 mg/L (HR 1.39, 95% CI 1.08-1.79) and, more strongly, high IL-6 (HR 1.92, 95% CI 1.64-2.23), each independently. In stratified analysis, hsCRP did not amplify Lp(a)'s mortality association, but high IL-6 conferred additional risk specifically at Lp(a) above 100 mg/dL (HR 1.25, 95% CI 1.09-1.44). The authors conclude markedly elevated Lp(a) carries greater mortality risk in the context of high IL-6-driven inflammation specifically, not hsCRP, suggesting anti-inflammatory treatments targeting the IL-6 pathway could offer added benefit in high-Lp(a) patients.
Original abstract
Objective: Lipoprotein(a) [Lp(a)] concentrations have been associated with cardiovascular risk. Recent studies suggested an interaction between systemic inflammation assessed via high-sensitivity C-reactive protein (hsCRP) and Lp(a). This study aimed to evaluate whether Lp(a), hsCRP, and interleukin-6 (IL-6) levels are associated with cardiovascular mortality in a German hospital-based cohort.
Methods: Data were drawn from the Ludwigshafen Risk and Cardiovascular Health (LURIC) study, including 3,316 patients undergoing coronary angiography. Lp(a) was measured by immunoturbidimetry and categorized into three strata (< 50 mg/dL, n = 2668; 50-100 mg/dL, n = 482; > 100 mg/dL, n = 163). HsCRP was measured by immunonephelometry and categorized by intervals (1st < 1 mg/L, 2nd 1-2 mg/L and 3rd interval > 2 mg/L). IL-6 was measured by ELISA and categorized into two groups (1st < 3.2 ng/L, 2nd ≥ 3.2 ng/L). The primary outcome was cardiovascular disease (CVD) mortality, analyzed using Cox proportional hazards models and logistic regression.
Results: Participants were predominantly male, with a mean age of 62.6 years. Extremely high Lp(a) (> 100 mg/dL) was associated with increased cardiovascular mortality (HR 1.5, 95% CI 1.06-2.12) compared to Lp(a) < 50 mg/dl. Both hsCRP (> 2 mg/L, HR 1.39, 95% CI 1.08-1.79 third vs. first interval) and more so IL-6 (HR 1.92, 95% CI 1.64-2.23, upper vs. lower half), were independently associated with higher CVD mortality. While hsCRP did not increase the Lp(a)-CVD mortality in stratified analysis, high IL-6 conferred an increased risk at Lp(a) levels > 100 mg/dL (HR 1.25, 95% CI 1.09-1.44).
Conclusion: HsCRP and IL-6 are associated with cardiovascular mortality. Markedly elevated Lp(a) is associated with an increased risk of cardiovascular mortality in the context of high systemic inflammation. Anti-inflammatory treatments may provide additional therapeutic benefits for individuals with high Lp(a).
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.