Hossa Jessica, McGuire Laura Stone, Valyi-Nagy Tibor, Abou-Mrad Tatiana, Theiss Peter, Tshibangu Mpuekela, Madapoosi Adrusht, Charbel Fady T, Alaraj Ali
Department of Surgery, University of Illinois Chicago, Chicago, Illinois, USA.
Department of Neurosurgery, University of Wisconsin-Madison, Madison, Wisconsin, USA.
World Neurosurg. 2025 Feb;194:123368. doi: 10.1016/j.wneu.2024.10.097. Epub 2024 Nov 20.
Endothelial dysfunction, induced by high shear stress from increased nidal blood flow, may promote a cycle of inflammation, possibly leading to instability and cerebral arteriovenous malformations (AVMs) rupture. Macrophages, identified with Cluster of Differentiation 68, are key inflammatory components in AVM pathology. We aim to evaluate the relationship of inflammation with AVM flow and hemosiderin.
This is a retrospective study of archived tissue. Adult patients (2002-2022) with baseline quantitative magnetic resonance angiography imaging, no embolization, and history of microsurgical resection (n = 17), with both ruptured (n = 9) and unruptured cases (n = 8). Brain AVM sections were stained with Cluster of Differentiation 68 to quantify vessel wall macrophage infiltration and hematoxylin and eosin stain as a control and to quantify hemosiderin. Quantitative magnetic resonance angiography with noninvasive optimal vessel analysis was reviewed, and AVM flow was calculated. Statistical analyses were performed.
There were no significant differences among macrophage infiltration and patient demographics, Spetzler-Martin grade, eloquence, venous stenosis, nidus compactness, volume, and AVM flow. Vessel wall macrophage infiltration positively correlated with patients who presented with confirmed AVM rupture (163.8 ± 46.7 vs. 101.3 ± 49.4, P = 0.017). Increases in vessel wall macrophage infiltration were found to positively correlate with higher grades of hemosiderin (P = 0.023), except for grade 4 hemosiderin. Venous anomaly showed a negative association with macrophage infiltration (P = 0.035).
These findings suggest a relationship among AVM vessel wall inflammation, hemosiderin, and hemorrhage presentation. Further investigations with larger sample sizes are warranted to understand the role of altered hemodynamics, hemosiderin deposition, and inflammation in AVM vessel walls.
由巢状血流量增加引起的高剪切应力所诱导的内皮功能障碍，可能会促进炎症循环，这可能会导致脑动静脉畸形（AVM）不稳定并破裂。通过分化簇68鉴定的巨噬细胞是AVM病理中的关键炎症成分。我们旨在评估炎症与AVM血流和含铁血黄素之间的关系。
这是一项对存档组织的回顾性研究。纳入2002年至2022年的成年患者（n = 17），这些患者有基线定量磁共振血管造影成像、未进行栓塞且有显微手术切除史，包括破裂病例（n = 9）和未破裂病例（n = 8）。脑AVM切片用分化簇68染色以量化血管壁巨噬细胞浸润情况，并用苏木精和伊红染色作为对照以量化含铁血黄素。回顾了采用无创最佳血管分析的定量磁共振血管造影，并计算AVM血流量。进行了统计分析。
巨噬细胞浸润与患者人口统计学特征、斯佩茨勒 - 马丁分级、功能区、静脉狭窄、巢状致密性、体积和AVM血流量之间无显著差异。血管壁巨噬细胞浸润与确诊为AVM破裂的患者呈正相关（163.8 ± 46.7 vs. 101.3 ± 49.4，P = 0.017）。发现血管壁巨噬细胞浸润增加与更高等级的含铁血黄素呈正相关（P = 0.023），4级含铁血黄素除外。静脉异常与巨噬细胞浸润呈负相关（P = 0.035）。
这些发现表明AVM血管壁炎症、含铁血黄素和出血表现之间存在关联。有必要进行更大样本量的进一步研究，以了解血流动力学改变、含铁血黄素沉积和炎症在AVM血管壁中的作用。
