Targeting Cerebral Arteriovenous Malformations for Minimally Invasive Therapy

Abstract

Cerebral arteriovenous malformation (AVM) embolization has been performed for nearly 40 years to reduce the risk of hemorrhage, to reduce symptomatic arteriovenous shunting, and to pretreat patients for surgical excision or radiosurgery. In some cases, embolization alone may be able to angiographically cure an AVM, although this is a small percentage of all AVMs. This report reviews the current limitations of embolic therapy of cerebral AVMs from the standpoint of AVM angioarchitecture and the physical limitations of current embolic materials. In addition, it seeks to identify the areas in which embolization therapy may make advancements both as a pretreatment and as a sole therapy. Currently, liquid embolic agents, ethylene vinyl alcohol, and n-butylcyanoacrylate seem to provide the greatest resistance to recanalization in AVM embolization. These agents, however, elicit only a weak, nonspecific, bioactive inflammatory response by histopathology. The further evaluation and understanding of the vascular biology of AVM vessels and the endothelium cell wall biology will help us devise more bioactive material solutions to AVM nidus obliteration. Targeting specific receptors in AVMs with the embolic material delivered may additionally enhance the effects of radiosurgery in these patients.