Beta-Blocker Utilization in Intracranial Arteriovenous Malformations: A Narrative Review of Current Evidence,...

Background/Objective: Intracranial arteriovenous malformations (AVMs) are high-flow cerebrovascular lesions associated with a significant risk of intracranial hemorrhage, neurological morbidity, and mortality. Current management strategies, including microsurgical resection, endovascular embolization, stereotactic radiosurgery, and conservative observation, remain limited by procedural risk and uncertain long-term outcomes. Beta-blockers, particularly propranolol, have recently attracted interest as potential adjunctive therapies because of their vasoconstrictive, antiangiogenic, and vascular remodeling properties. This review evaluates the mechanistic rationale and current evidence regarding beta-blocker use in intracranial AVMs. Methods: A comprehensive literature review was conducted using PubMed, Scopus, and Google Scholar databases through January 2026 using combinations of the terms "arteriovenous malformation," "AVM," "beta-blocker," "propranolol," "angiogenesis," "hemorrhage," and "cerebral cavernous malformation." Eligible studies included experimental investigations, translational studies, observational cohorts, case reports, clinical trials, systematic reviews, and meta-analyses evaluating beta-blocker use in intracranial AVMs or related vascular malformations. Studies unrelated to cerebrovascular lesions, duplicate reports, and non-English publications were excluded. Given the heterogeneity and limited volume of available AVM-specific literature, findings were synthesized narratively rather than through formal systematic review methodology. Discussion: Preclinical studies suggest that beta-blockers modulate molecular pathways implicated in AVM pathophysiology, including VEGF, HIF-1α, SDF1α/CXCR4, MMP-9, and Notch-associated signaling. These mechanisms may reduce abnormal angiogenesis, endothelial instability, and pathological vascular remodeling. Clinical evidence, however, remains limited to retrospective studies, perioperative reports, and indirect evidence from cerebral cavernous malformations. Observational studies have reported associations between beta-blocker exposure and certain favorable AVM characteristics, including lower rates of hemorrhagic presentation and less complex angioarchitecture. However, these findings are highly susceptible to confounding, reverse causation, and selection bias and should not be interpreted as evidence of disease modification. Conclusions: Beta-blockers cannot currently be recommended as definitive therapy for intracranial AVMs. Their established role remains perioperative hemodynamic control, while potential disease-modifying effects require validation through prospective studies and randomized clinical trials.