The Correlation of Vessel Wall Macrophage Infiltration With Hemosiderin in Arteriovenous Malformations

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.