Department of Neurosurgery, Radboud University Medical Center, Nijmegen, The Netherlands
Department of Neurosurgery, Radboud University Medical Center, Nijmegen, The Netherlands.
J Neurointerv Surg. 2020 Nov;12(11):1117-1121. doi: 10.1136/neurintsurg-2019-015753. Epub 2020 Apr 24.
Inflammation-related factors might give further insight into the pathophysiology of vessel wall inflammation and intracranial aneurysm (IA) rupture. One of these factors is the protein complex S100A8/A9, which is released by neutrophils, monocytes, and activated macrophages and is known for its role in cardiovascular disease.
To determine if venous S100A8/A9 levels in patients with a ruptured IA (rIA) or unruptured IA (uIA) are elevated compared with a control group. Second, to assess differences between venous and intra-aneurysmal S100A8/A9 levels of rIA and uIA patients.
A prospective case study was performed between June 2016 and May 2017 in patients harboring a ruptured or unruptured saccular IA. Primary outcome measures were individual S100A8/A9 serum concentrations as measured in venous and intra-aneurysmal blood samples during endovascular treatment. Venous serum S100A8/A9 concentrations from a healthy control group served as a reference.
We included 16 patients with either a rIA or uIA and 47 healthy controls. Venous S100A8/A9 concentrations were higher in aneurysm patients (rIA and uIA) than those of healthy controls (P≤0.001). S100A8/A9 concentrations were higher in intra-aneurysmal samples than in venous samples of rIA patients (P=0.011). This difference was not found in uIA patients (P=0.054). Intra-aneurysmal S100A8/A9 levels were higher in rIAs than in uIAs (P=0.04).
Venous S100A8/A9 levels are elevated in patients with both rIAs and uIAs compared with healthy controls and likely represents aneurysm wall inflammation. S100A8/A9 causes macrophage-induced inflammation and degeneration of the vessel wall which might explain higher intra-aneurysmal S100A8/A9 levels found in rIAs than in uIAs.
与颅内动脉瘤（IA）破裂相关的炎症相关因素可能进一步深入了解血管壁炎症和颅内动脉瘤破裂的病理生理学。其中一个因素是 S100A8/A9 蛋白复合物，它由中性粒细胞、单核细胞和活化的巨噬细胞释放，其在心血管疾病中的作用已得到证实。
确定破裂性颅内动脉瘤（rIA）或未破裂性颅内动脉瘤（uIA）患者的静脉 S100A8/A9 水平是否高于对照组。其次，评估 rIA 和 uIA 患者静脉和瘤内 S100A8/A9 水平之间的差异。
本研究为 2016 年 6 月至 2017 年 5 月期间的前瞻性病例研究，研究对象为患有破裂或未破裂的囊状 IA 的患者。主要观察指标为血管内治疗期间静脉和瘤内血液样本中单个 S100A8/A9 血清浓度。健康对照组的静脉血清 S100A8/A9 浓度作为参考。
共纳入 16 例 rIA 或 uIA 患者和 47 例健康对照者。与健康对照组相比，动脉瘤患者（rIA 和 uIA）的静脉 S100A8/A9 浓度更高（P≤0.001）。rIA 患者的瘤内样本 S100A8/A9 浓度高于静脉样本（P=0.011）。而在 uIA 患者中则未发现这种差异（P=0.054）。rIA 患者的瘤内 S100A8/A9 水平高于 uIA 患者（P=0.04）。
与健康对照组相比，rIA 和 uIA 患者的静脉 S100A8/A9 水平升高，可能代表动脉瘤壁炎症。S100A8/A9 引起巨噬细胞诱导的炎症和血管壁退化，这可能解释了 rIA 瘤内 S100A8/A9 水平高于 uIA 的原因。
