Preoperative statin therapy reduces new ischemic cerebral infarction after intracranial aneurysm stent placement independently of baseline LDL-C level

医学 他汀类 神经血管束 内科学 心脏病学 动脉瘤 脑梗塞 支架 梗塞 缺血 基线(sea) 放射科 外科
作者
Qichen Peng,Yangyang Zhou,Xuanping Xie,Linggen Dong,Zhu Xq,K. L. Liu,Junfan Chen,Xiaofei Huang,Yang Wang,Shiqing Mu,Xia Yang,W M Li
出处
期刊:Journal of NeuroInterventional Surgery [BMJ]
卷期号:: jnis-2025
标识
DOI:10.1136/jnis-2025-024677
摘要

BACKGROUND: New ischemic cerebral infarction (NICI) on diffusion-weighted imaging (DWI) is frequently observed after stent-assisted coiling. OBJECTIVE: To investigate whether preoperative statin use reduces NICI volume and whether the effect depends on baseline low-density lipoprotein cholesterol (LDL-C). METHODS: We retrospectively analyzed 490 patients with intracranial aneurysms who underwent stent-assisted treatment at multiple centers. Based on preoperative statin use, patients were classified into statin (n=269) and non-statin (n=221) groups. NICI volume was quantified on postoperative DWI. Multivariable linear regression was used to identify predictors of log-transformed NICI volume, including an interaction term between statin use and LDL-C >3.4 mmol/L. RESULTS: Median infarct volume was significantly lower in the statin group (1.39 (IQR 0.87-1.92)) than in the non-statin group (1.83 (IQR 1.48-2.47); P<0.001). After multivariable adjustment, statin use remained independently associated with smaller NICI volume (B = -0.382; 95% CI -0.488 to -0.277; P<0.001). Subgroup analysis showed consistent reductions in both statin+normal LDL-C and statin+high LDL-C subgroups (both P<0.001). No interaction was observed between statin use and LDL-C level (P=0.147), suggesting consistent protection regardless of lipid status. Smoking (B=0.407; P<0.001), higher body mass index (B=0.040; P<0.001), and female sex (B=0.130; P=0.033) were independent predictors of larger infarct volume. CONCLUSIONS: Preoperative statin therapy significantly reduced NICI volume after stent-assisted aneurysm treatment, independently of LDL-C, suggesting possible neurovascular protection through pleiotropic mechanisms beyond lipid lowering.
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