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Systemic inflammation modulates lipoprotein(a)-associated coronary stenosis in the chronic coronary syndromes
Lu Shen1,2, Wenqing Zhai1, Ping Jiang3
1Department of Health Promotion and Behavioural Sciences, School of Public Health, Anhui Medical University, No.69 Meishan Road, Shushan District, Hefei, Anhui Province, China.
Insights
Elevated lipoprotein(a) [Lp(a)] increases coronary stenosis risk, but only when systemic inflammation is low. Personalized therapies for chronic coronary syndromes (CCS) should consider inflammation levels for effective Lp(a) management.
Area of Science:
- Cardiology
- Inflammation Research
- Vascular Biology
Background:
- Lipoprotein(a) [Lp(a)] levels and associated cardiovascular risk are linked to systemic inflammation.
- Investigating the role of systemic inflammation in modulating Lp(a)-associated coronary stenosis in chronic coronary syndromes (CCS) is crucial.
Purpose of the Study:
- To determine if systemic inflammation influences the relationship between lipoprotein(a) and coronary stenosis severity in patients with chronic coronary syndromes.
- To explore the impact of varying inflammation levels on Lp(a)-associated coronary artery disease risk.
Main Methods:
- A retrospective, cross-sectional study of 1513 patients undergoing coronary angiography.
- Patients were stratified by coronary stenosis severity using Gensini Scores and categorized by systemic inflammation levels (SIRI, SII, NLR).
- Multinomial logistic regression models were employed to analyze the association between Lp(a) and stenosis under different inflammatory conditions.
Main Results:
- Elevated Lp(a) was significantly associated with increased coronary stenosis risk (mild and severe) in the overall cohort.
- This association was most pronounced in patients with low systemic inflammation (SIRI < 0.64), with significantly higher odds of mild and severe stenosis.
- No significant association between Lp(a) and coronary stenosis was observed in patients with moderate or high systemic inflammation.
Conclusions:
- The correlation between elevated lipoprotein(a) and coronary stenosis is contingent upon low systemic inflammation levels.
- Personalized therapeutic strategies targeting Lp(a) in chronic coronary syndromes should incorporate assessments of the patient's inflammatory status for optimal management.
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.
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