Can Induction of Systemic Hypotension Help Prevent Nidus Rupture Complicating Arteriovenous Malformation Embolization?: Analysis of Underlying Mechanisms Achieved Using a Theoretical Model
Tarik F. Massoud
,a,
George J. Hademenosa,
William L. Younga,
Erzhen Gaoa and
John Pile-Spellmana
a From the Division of Interventional Neuroradiology and Department of Radiological Sciences (T.F.M., G.J.H.), University of California at Los Angeles School of Medicine, Los Angeles; Departments of Radiology (T.F.M., W.L.Y., J.P.-S.), Anesthesiology (W.L.Y.), and Neurological Surgery (W.L.Y., J.P.-S.), College of Physicians and Surgeons, and the Department of Electrical Engineering (E.G.), Columbia University, New York, New York.
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FIG 1. Schematic diagram of the electrical network describing the biomathematical AVM hemodynamic model. CCA, common carotid artery; ECA, external carotid artery; ICA, internal carotid artery; SCA, subclavian artery; VA, vertebral artery; PCA, posterior cerebral artery; ACA, anterior cerebral artery; MCA, middle cerebral artery; E, electromotive force; N, node; L, loop; i, blood flow; R, resistance; SP, systemic pressure, AF, arterial feeder; DV, draining vein; CVP, central venous pressure. (Reproduced with permission of authors and publisher, reference 4)
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FIG 2. Schematic diagram of a portion of the electrical network AVM model to show the effects of extranidal rerouting of blood pressure after incomplete nidus occlusion with embolic glue (mechanism 2). Panel A: Features of the normal AVM model prior to simulated embolization. Note normal mean pressures in vessels i7 (47 mm Hg), i6 (66 mm Hg), i2 (66 mm Hg), and i1 (47 mm Hg) that form a loop outside the nidus. Panels B to E: Progressive partial occlusion of the nidus with simulated glue (gray) when embolization is achieved via AF2. Note changes in values of mean pressures in the extranidal loop and resulting rupture of nidus vessel i21 (checkered vessel in B and C) and nidus vessel i37 (checkered vessel in D and E)
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FIG 3. Line diagram representing mean blood pressure drops across the theoretical AVM according to position within the circulation. At normotension, mean systemic pressure is 74 mm Hg. When systemic hypotension is induced in the circulation, the mean systemic pressure falls to 70 mm Hg (minor hypotension), 50 mm Hg (moderate hypotension), or 25 mm Hg (profound hypotension)
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FIG 4. Graph to show how injection pressures (that are in addition to the baseline intravascular pressures) in intranidal vessels i21 and i37 (when an injection is performed through AF1), and in vessel i12 (when an injection is performed through AF2) affect the risk of rupture of these vessels. Vessels i21 and i37 rupture (risk >100%) with high injection pressures
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FIG 5. 3D bar chart to show changes in risk of rupture for intranidal vessels i21 (dark columns) and i37 (light columns), both of which were found to rupture after extranidal rerouting of pressure consequent to partial embolization via AF1 (mechanism 2, as in fig 2). B to E represent extent of progressive nidus occlusion as depicted in figure 2. Note that both vessels rupture (risk >100%) at systemic normotension (74 mm Hg). The reduction in risk of rupture occurs with moderate systemic hypotension (50 mm Hg) and is more pronounced at profound systemic hypotension (25 mm Hg)
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