Journal of inflammation research · 2026
Associations of Systemic Inflammatory Response Index (SIRI) and Systemic Inflammatory Index (SII) with Cerebral Atherosclerosis.
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Yang Chunjiao, Cai Qi, Xie Yu, Luo Lei, Huang Yinfei, Zhang Renwei, Liu Yumin
Аннотация
BACKGROUND: Atherosclerosis is a chronic inflammatory disease and a leading cause of stroke. Systemic inflammatory biomarkers are recognized predictors of coronary artery disease. However, their association with cerebral atherosclerosis remains unclear. This study aims to investigate the relationship between systemic inflammatory indices and cerebral atherosclerotic burden.
METHODS: A cohort of 5444 patients was enrolled. Cerebral atherosclerotic stenosis was evaluated using DSA, CTA, or MRA. The systemic inflammation response index (SIRI) and systemic immune-inflammation index (SII) were calculated and natural-log-transformed (ln-SIRI, ln-SII). The associations of ln-SIRI and ln-SII with the presence, severity (maximal stenosis degree) and extent (number of lesions) of cerebral atherosclerosis were evaluated using binary logistic regression, ordered logistic regression and restricted cubic spline models. Subgroup analyses were further conducted across clinically relevant strata to assess the consistency of these associations. Additionally, the diagnostic performance of both indices was evaluated using receiver operating characteristic (ROC) curve analysis.
RESULTS: Patients with cerebral atherosclerotic stenosis had significantly higher ln-SIRI (OR: 1.27, 95% CI: 1.19-1.35) and ln-SII (OR: 1.22, 95% CI: 1.15-1.30) compared to the non-stenosis group (both p < 0.001). Both indices showed significant positive associations with the severity of the most stenotic lesion (ln-SIRI OR: 1.29, 95% CI: 1.22-1.36; ln-SII OR: 1.26, 95% CI: 1.20-1.33) and the number of affected sites (ln-SIRI OR: 1.27, 95% CI: 1.20-1.34; ln-SII OR: 1.24, 95% CI: 1.18-1.31), suggesting a significant graded association (p for trend < 0.001). Restricted cubic spline analyses revealed linear associations of ln-SIRI and ln-SII with cerebral atherosclerosis presence, severity and extent. In subgroup analyses stratified by age, comorbidities, and imaging modality, these associations remained consistent (all subgroup p < 0.05). ROC analysis indicated that both indices had modest discriminatory ability, with AUCs of 0.699 for ln-SIRI and 0.698 for ln-SII.
CONCLUSION: The systemic inflammatory indices ln-SIRI and ln-SII are significantly associated with the presence, severity and extent of cerebral atherosclerosis. These easily obtainable biomarkers may hold promise for improving risk stratification in cerebrovascular diseases.
METHODS: A cohort of 5444 patients was enrolled. Cerebral atherosclerotic stenosis was evaluated using DSA, CTA, or MRA. The systemic inflammation response index (SIRI) and systemic immune-inflammation index (SII) were calculated and natural-log-transformed (ln-SIRI, ln-SII). The associations of ln-SIRI and ln-SII with the presence, severity (maximal stenosis degree) and extent (number of lesions) of cerebral atherosclerosis were evaluated using binary logistic regression, ordered logistic regression and restricted cubic spline models. Subgroup analyses were further conducted across clinically relevant strata to assess the consistency of these associations. Additionally, the diagnostic performance of both indices was evaluated using receiver operating characteristic (ROC) curve analysis.
RESULTS: Patients with cerebral atherosclerotic stenosis had significantly higher ln-SIRI (OR: 1.27, 95% CI: 1.19-1.35) and ln-SII (OR: 1.22, 95% CI: 1.15-1.30) compared to the non-stenosis group (both p < 0.001). Both indices showed significant positive associations with the severity of the most stenotic lesion (ln-SIRI OR: 1.29, 95% CI: 1.22-1.36; ln-SII OR: 1.26, 95% CI: 1.20-1.33) and the number of affected sites (ln-SIRI OR: 1.27, 95% CI: 1.20-1.34; ln-SII OR: 1.24, 95% CI: 1.18-1.31), suggesting a significant graded association (p for trend < 0.001). Restricted cubic spline analyses revealed linear associations of ln-SIRI and ln-SII with cerebral atherosclerosis presence, severity and extent. In subgroup analyses stratified by age, comorbidities, and imaging modality, these associations remained consistent (all subgroup p < 0.05). ROC analysis indicated that both indices had modest discriminatory ability, with AUCs of 0.699 for ln-SIRI and 0.698 for ln-SII.
CONCLUSION: The systemic inflammatory indices ln-SIRI and ln-SII are significantly associated with the presence, severity and extent of cerebral atherosclerosis. These easily obtainable biomarkers may hold promise for improving risk stratification in cerebrovascular diseases.