Hypertensive Hemodynamics in Type II Endoleak: Unveiling Biomechanical Pathways to Thrombosis Impediment and Aneurysm Destabilization via FSI Simulation.

Hypertension is a key risk factor for type II endoleaks after endovascular aneurysm repair (EVAR), but the biomechanical mechanisms linking blood pressure to outcomes are unclear. This study aimed to elucidate these mechanisms by examining how elevated branching vessel pressure affects sac hemodynamics and wall mechanics. This study constructed a type II endoleak model with a patent inferior mesenteric artery (IMA) and two lumbar arteries (LAs). The non-Newtonian fluid model and a two-way fluid-structure interaction (FSI) method were utilized to simulate the blood flow and vessel wall mechanics for type II endoleak. By setting different inlet pressures for the branching vessels, this study investigated the impact of blood pressure on the biomechanical environment following EVAR. An increase in IMA and LA inlet pressures led to a reversal of blood flow at the branch vessels and resulted in an unstable flow field within the aneurysm sac. This was accompanied by elevated wall shear stress (WSS), energy loss (EL), sac wall displacement, and Von Mises stress. The pressure within the aneurysm sac also rose correspondingly. Elevated inlet pressures in the IMA and LA lead to increased and prolonged retrograde flow into the aneurysm sac, elevate sac pressure, raise WSS and EL, and amplify wall displacement and mechanical stress-collectively intensifying hemodynamic disturbance and structural loading on the aneurysm wall.