Inflammation
Lp(a)'s link to coronary stenosis holds only under low systemic inflammation, 1,513-patient angiography study finds (Am J Prev Cardiol 2025)
Original title: Systemic inflammation modulates lipoprotein(a)-associated coronary stenosis in the chronic coronary syndromes
This retrospective cross-sectional study analysed 1,513 participants undergoing coronary angiography at a tertiary centre in China, testing whether systemic inflammation modulates the association between Lp(a) and coronary stenosis severity (graded by Gensini score into normal, mild and severe groups). Overall, elevated Lp(a) predicted higher stenosis risk (fully adjusted OR 1.47, 95% CI 1.11-1.96 for mild vs. normal; OR 1.68, 95% CI 1.21-2.33 for severe vs. normal). Stratifying by the systemic inflammation response index (SIRI), this Lp(a)-stenosis association persisted only in the low-inflammation group (SIRI below 0.64: OR 2.03, 95% CI 1.17-3.54, P = 0.012 for mild; OR 2.34, 95% CI 1.24-4.44, P = 0.009 for severe), with no significant association at moderate or high inflammation; the systemic immune-inflammation index and neutrophil-to-lymphocyte ratio gave consistent results. The authors argue background inflammatory burden should be factored into personalised Lp(a)-lowering strategies for chronic coronary syndromes.
Original abstract
Background: Recent researches highlight the interdependence of lipoprotein(a) [Lp(a)] and Lp(a)-associated cardiovascular risk with the background inflammatory burden. This study aimed to investigate whether systemic inflammation modulates Lp(a)-associated coronary stenosis in chronic coronary syndromes (CCS).
Methods: A total of 1513 participants undergoing angiography at a tertiary cardiology center in China were included in our retrospective, cross-sectional study. Participants were categorized into normal, mild, and severe groups based on the Gensini Scores, which quantitatively assess stenosis severity. Multinomial logistic models were calculated according to accompanying systemic inflammation concentration.
Results: Participants with elevated Lp(a) levels had a high coronary stenosis risk: fully adjusted model odds ratios (ORs) [95% confidence intervals (CIs)] for the mild vs. normal and severe vs. normal groups were 1.47 (1.11-1.96) and 1.68 (1.21-2.33). Notably, the strongest Lp(a)-coronary stenosis associations after multi-variable adjustment persisted only in low inflammation concentration [systemic inflammation response index (SIRI) < 0.64)] [mild vs. normal, OR 2.03, 95% CI 1.17-3.54, P = 0.012; severe vs. normal, OR 2.34, 95% CI 1.24-4.44, P = 0.009], with no associations in moderate (0.64 ≤ SIRI < 1.41) and high (SIRI ≥ 1.41) state. Identical analysis across the systemic immune-inflammation index (SII) and neutrophil to lymphocyte ratio (NLR) yielded consistent results.
Conclusions: Elevated Lp(a) correlates with coronary stenosis only in low inflammation concentration. Considering systemic inflammation in personalized Lp(a)-lowering therapies is more conducive for CCS managements.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.