Association Between the Systemic Immune-Inflammation Index and Aneurysmal Wall Enhancement on High-Resolution
Jiwan Huang1, Runze Ge1, Caihong Li2
1Neurosurgery Center, Department of Cerebrovascular Surgery, The National Key Clinical Speciality, Engineering Research Center of Diagnostic and Therapeutic Technology and Devices for Cerebrovascular Diseases, Ministry of Education, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Zhujiang Hospital Institute for Brain Science and Intelligence, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Background:
Inflammation is a critical driver of intracranial aneurysm (IA) instability. The systemic immune-inflammation index (SII), a novel composite inflammatory biomarker, may reflect the local mural changes observed on vessel wall imaging (VWI).
Purpose/Hypothesis:
To investigate the association between the SII and aneurysmal wall enhancement (AWE) on high-resolution vessel wall imaging (HRVWI), and to evaluate SII as a potential biomarker for aneurysm instability.
Study Type:
Prospective cross-sectional study.
Population:
Four hundred and eighteen intracranial aneurysms in 311 patients (65.3% female, median age 58.0 years) underwent HRVWI. A sub-cohort of 67 patients with 84 aneurysms was included for longitudinal analysis of aneurysm growth (median follow-up 7.0 months).
Field Strength/Sequence:
Field strength/sequence: A 3.0T MR scanner; 3D time-of-flight magnetic resonance angiography (TOF-MRA); 3D black-blood T1-weighted volumetric turbo spin echo acquisition (T1-VISTA); and post-contrast vessel wall imaging using a 3D fast field echo sequence.
Assessment:
AWE defined as aneurysm-to-pituitary stalk contrast ratio (CRstalk) ≥ 0.60. SII was calculated from admission blood counts as (platelet count * neutrophil count)/(lymphocyte count * 1000).
Statistical Tests:
Multivariable logistic regression and propensity score matching evaluated the association between SII and AWE. Longitudinal analysis was performed using Firth's logistic regression. Subgroup analyses were stratified by clinical and aneurysmal characteristics. p < 0.05 was considered significant.
Results:
AWE was present in 142/418 (34.0%) aneurysms. In multivariable analysis, elevated SII was independently associated with AWE (odds ratio [OR] = 1.93). This association remained significant after PSM (median SII: 0.60 in AWE group vs. 0.42 in non-AWE group). SII was also independently associated with aneurysm growth in the longitudinal sub-cohort (OR = 20.519). Subgroup analysis showed a significant interaction with aneurysm location, with the strongest association in the internal carotid artery (OR = 3.55; 95% CI: 1.63-7.71).
Data Conclusion:
Elevated SII is independently associated with the presence of AWE and aneurysm growth.
Evidence Level:
3.
Technical Efficacy:
Stage 2.
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