Abstract
There are currently no in vivo techniques to accurately study dynamic equilibrium of blood flow within separate regions (compartments) of a large brain arteriovenous malformation (AVM) nidus. A greater understanding of this AVM compartmentalization, even if theoretical, would be useful for optimal planning of endovascular and multimodal AVM therapies. We aimed to develop a biomathematical AVM model for theoretical investigations of intranidal regions of increased mean intravascular pressure (Pmean) and flow representing hemodynamic compartments, upon simulated AVM superselective angiography (SSA). We constructed an AVM model as a theoretical electrical circuit containing four arterial feeders (AF1–AF4) and a three-dimensional nidus of 97 interconnected plexiform and fistulous components. We simulated SSA by increases in Pmean in each AF (with and without occlusion of all other AFs), and then used network analysis to establish resulting increases in Pmean and flow within each nidus vessel. We analyzed shifts in hemodynamic compartments consequent to increasing AF injection pressures. SSA simulated by increases of 10 mm Hg in AF1, AF2, AF3, or AF4 resulted in dissipation of Pmean over 38, 66, 76, or 20% of the nidus, respectively, rising slightly with simultaneous occlusion of other AFs. We qualitatively analyzed shifting intranidal compartments consequent to varying injection pressures by mapping the hemodynamic changes onto the nidus network. Differences in extent of nidus filling upon SSA injections provide theoretical evidence that hemodynamic and angioarchitectural features help establish AVM nidus compartmentalization. This model based on a theoretical AVM will serve as a useful computational tool for further investigations of AVM embolotherapy strategies.
Highlights
A brain arteriovenous malformation (AVM) is a congenital abnormal tangle of dilated blood vessels in the brain that directly diverts blood from arteries to veins, and in doing so, bypasses normal brain tissue
Hemodynamic simulations within the computational AVM model in its baseline state prior to simulated superselective angiography (SSA) revealed a total volumetric blood flow of 678 mL/min through the nidus akin to values obtained in large cerebral AVMs (Yamada et al, 1993), with markedly increased flow through the intranidal fistula
We believe that the modeling process we present should act as a stimulus for further study of human AVM nidus biophysical, morphological, and morphometric characteristics that could be implemented in future more clinically relevant AVM models to guide clinical decision making
Summary
A brain arteriovenous malformation (AVM) is a congenital abnormal tangle (nidus) of dilated blood vessels in the brain that directly diverts blood from arteries (or arterial feeders [AFs]) to veins (or draining veins [DVs]), and in doing so, bypasses normal brain tissue. The two hallmarks of AVMs are the presence of a nidus and the associated hemodynamic shunting of arterial blood. Computational Modeling of Brain AVM Compartments at high pressure through the nidus and directly into DVs, without the resistance normally offered by brain capillaries. Within any large AVM nidus, a dynamic equilibrium of blood flow exists in separate regions, or compartments, that are each supplied by their own AF (Massoud and Hademenos, 1999; Kakizawa et al, 2002). A greater theoretical understanding of the nature of AVM hemodynamic compartmentalization would be useful for optimal planning of endovascular and multimodal AVM treatments
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