目的:颅内动脉粥样硬化性狭窄(ICAS)是全球缺血性卒中的主要原因。高脂血症是动脉粥样硬化的主要原因。然而,高脂血症对颅内动脉粥样硬化斑块演变和下游缺血发作的影响尚不清楚.在这项研究中,我们旨在评估ICAS斑块的影像学特征,并探讨高脂血症与斑块进展之间的关系.
方法:我们纳入了接受高分辨率磁共振成像的ICAS患者(狭窄≥50%)。罪犯牌匾被定义为鞋底,或者在多发性狭窄的情况下,导致急性缺血性卒中的颅内动脉最窄的斑块。人口统计,临床资料,MRI上的斑块特征,比较了罪犯和非罪犯斑块之间的脂质参数。通过在T1加权序列上进行对比增强后与相邻的正常血管壁和垂体漏斗进行比较,斑块增强分级为0、1和2级。
结果:纳入162例患者(平均年龄57.7±12.1岁,男性61.6%),其中110人被确定为同侧急性中风的罪魁祸首斑块。高级别增强是可定罪斑块最突出的MRI特征(Grade-2:OR6.539,95CI1.706-23.707,p=0.006)。LDL胆固醇与罪犯斑块引起的整体急性缺血性卒中显著相关。通过增强分级分层后,LDL与1级增强斑块的缺血事件独立相关(OR6.778,95CI2.122-21.649,p=0.001)。在2级增强斑块的患者中,然而,LDL与缺血事件无关;相反,中性粒细胞/淋巴细胞比率与2级增强斑块引起的缺血事件独立相关(OR2.188,95CI1.209-3.961,p=0.010)。
结论:LDL与颅内动脉粥样硬化斑块进展中期的缺血事件有关,强化降脂治疗的最佳时期。在高级阶段,炎症因子可能是导致缺血事件的主要因素.
OBJECTIVE: Intracranial atherosclerotic stenosis (ICAS) is the leading cause of ischemic stroke worldwide. Hyperlipidemia is a major contributor to atherosclerosis. However, the effect of hyperlipidemia on the evolution of intracranial atherosclerotic plaques and downstream ischemic episodes remains unclear. In this study, we aimed to assess the radiological features of ICAS plaques and to explore the relationship between hyperlipidemia and plaque progression.
METHODS: We included people with ICAS (≥50% stenosis) undergoing high-resolution magnetic resonance imaging. The culprit plaque was defined as the sole, or in case of multiple stenosis, the narrowest plaque on the intracranial artery responsible for acute ischemic stroke. Demographic, clinical data, plaque features on MRI, and lipid parameters were compared between culprit and non-culprit plaques. Plaque enhancement was graded as Grade 0, 1 and 2 by comparing to the adjacent normal vessel wall and pituitary funnel after contrast enhancement on T1-weighted sequences.
RESULTS: 162 patients were included (mean age 57.7±12.1 years, male 61.6%), 110 of whom were identified as culprit plaque with an ipsilateral acute stroke. High-grade enhancement was the most prominent MRI feature of the culpable plaque (Grade-2: OR 6.539, 95%CI 1.706-23.707, p=0.006). LDL cholesterol was significantly associated with overall acute ischemic stroke caused by culprit plaque. After stratification by enhancement grading LDL was independently associated with ischemic events in Grade-1 enhancement plaques (OR 6.778, 95%CI 2.122-21.649, p=0.001). In patients with Grade-2 enhancement plaques, however, LDL was not associated with ischemic event; in contrast, Neutrophil/Lymphocyte ratio was independently associated with ischemic events caused by Grade-2 enhancement plaques (OR 2.188, 95%CI 1.209-3.961, p=0.010).
CONCLUSIONS: LDL was related with ischemia events in intermediate stage of intracranial atherosclerotic plaque progression, an excellent period for intensive lipid-lowering treatment. In advanced stage, inflammatory agents maybe the main contributor to ischemic events.