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

• Published in: World neurosurgery
• Main Authors: Hossa, Jessica, McGuire, Laura Stone, Valyi-Nagy, Tibor, Abou-Mrad, Tatiana, Theiss, Peter, Tshibangu, Mpuekela, Madapoosi, Adrusht, Charbel, Fady T, Alaraj, Ali
• Format: Journal Article
• Language: English
• Published: 04.11.2024
• ISSN: 1878-8769; 1878-8769
• DOI: 10.1016/j.wneu.2024.10.097

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 CD68, are key inflammatory components in AVM pathology. We aim to evaluate the relationship of inflammation with AVM flow and hemosiderin.INTRODUCTIONEndothelial 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 CD68, 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 (QMRA) 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 CD68 to quantify vessel wall macrophage infiltration and hematoxylin and eosin stain as a control and to quantify hemosiderin. QMRA with noninvasive optimal vessel analysis (NOVA) was reviewed, and AVM flow was calculated. Statistical analyses were performed.METHODSThis is a retrospective study of archived tissue. Adult patients (2002-2022) with baseline quantitative magnetic resonance angiography (QMRA) 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 CD68 to quantify vessel wall macrophage infiltration and hematoxylin and eosin stain as a control and to quantify hemosiderin. QMRA with noninvasive optimal vessel analysis (NOVA) was reviewed, and AVM flow was calculated. Statistical analyses were performed.There were no significant differences between 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).RESULTSThere were no significant differences between 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 between 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.CONCLUSIONThese findings suggest a relationship between 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.