Abstract W P106: A 3D Computational Model of the Hemodynamic Changes in EC-IC Bypass With Physiologic Boundary Conditions
Introduction: Intracranial arterial stenosis (IAS) accounts for 10% of ischemic strokes. EC-IC bypass trials have failed to show benefit of STA to MCA bypass over medical management, particularly for patients with severe stenosis rather than occlusion. These outcomes may be explained by retrograde flow from the bypass competing with flow through the stenosis, creating conditions at risk for thrombosis, such as stagnant or turbulent flow. We present a computational fluid dynamics model of EC-IC bypass extracted from patient images to demonstrate the hemodynamic effects of a bypass.
Methods: A 2D-to-3D reconstruction algorithm was used to extract the vascular geometry from biplane angiograms of a patient with STA-MCA bypass. Additional details, such as the anterior temporal branch and lenticulostriates (LSAs) were added. The model was modified with varying degrees of stenosis. The boundary conditions of the outlets were adjusted to account for cerebrovascular autoregulation by finding the steady state of an autoregulatory model. The ANSYS: Simulation Technology package was used to evaluate hemodynamic parameters at 70% and 90% stenosis.
Results: The 70% stenosis showed small pressure drop across the stenosis compared to the 90% stenosis (712Pa, 3618Pa). Flow velocity and wall shear stress (WSS) were substantially higher in the M1 segment distal to the lesion in the 70% stenosis model than in the 90% model (105cm/s, 27cm/s; 3.4Pa vs. 0.66Pa). Both models exhibited slow retrograde flow through the M2 segment (7cm/s, 10cm/s). Maximal turbulent kinetic energy (TKE) was higher in 70% stenosis model (0.00586m^2/s^2, 0.0012m^2/s^2).
Conclusions: EC-IC bypass causes competitive flow within the M1 and M2 segments resulting in near complete stagnation of flow in regions of the MCA with high WSS and TKE, a set of conditions at high risk for intra-arterial thrombosis.
Author Disclosures: M. Connolly: None. F. Scalzo: None. D.S. Liebeskind: None. N.R. Gonzalez: Research Grant; Significant; NIH K23NS079477-01A1, AHA 12PILT12760011.
This research has received full or partial funding support from the American Heart Association, Western States - Alaska, Arizona, California, Hawaii, Idaho, Montana, Nevada, Oregon, Utah, Washington.
- © 2014 by American Heart Association, Inc.