Modeling the Hemodynamic Initiation of Endothelial Dysfunction in Intracranial Aneurysms

Mentors

• 

  Christopher Chen

  Professor (BME, MSE)

• Freddy Suarez Rodriguez

Project Description

Intracranial aneurysms (IA) are present in approximately 3% of the adult population. Rupture is the primary risk associated with aneurysms, which produces aneurysmal subarachnoid hemorrhage, a stroke subtype with a fatality rate of roughly 45%. Despite this, no pharmacological therapy exists to prevent aneurysm formation, growth, or rupture. This therapeutic gap reflects an incomplete mechanistic understanding of how the hemodynamic environment at bifurcations initiates endothelial dysfunction that precedes aneurysm formation. two hemodynamic parameters are consistently implicated: elevated walls hear stress (wows) and wall sheer stress gradients., both of which peak in the flow accelaration zones flanking a bifurcation apex. methodology: defined levels of walls hear stress were appleid to human coronary artery endothelial cells using PROPEL, a motor driven channeled flow device that delivers controlled and tunable shear across range spanning physiological to aneurysm-relevant static to 100 den/cm2. cells were imaged and VE-cadherin was segmented using cell pose and per cell morphometrics were extracted with MorphoLibJ in Fiji. Idealized bifurcation geometries were constructed in Solidworks. with a 300 UM parent vessel branching into 240 UM daughter vessels. two geometries differing in bifurcation angle (80 degrees and 150 degrees) were simulated in ANSYS fluent, assuming steady, laminar, incompressible flow with water as the working fluid. no slip walls, .15 m/s at the parent inlet, with both daughter branches set as outlets at 0 Pa. Wall shear stress was extracted along the luminal surface tomb its distribution relative to the bifurcation apex.