Cardiovascular disease (CVD) remains the leading cause of mortality worldwide, with
atherosclerosis-driven stenoses significantly altering haemodynamic and influencing potential nanoparticle drug delivery outcomes. This study applies computational fluid dynamics (CFD) via
ANSYS FLUENT finite volume software, to two-dimensional stenosed arteries of varying severities (۳۰%, ۵۰%, ۷۰%) and shoulder lengths (۲, ۴, ۶ mm). Two regimes have been compared: a steady Newtonian baseline, where viscosity and velocity remain constant and a physiologically realistic pulsatile non-Newtonian Carreau regime incorporating shear-thinning viscosity and cardiac-cycle effects. In the steady Newtonian simulations, velocity plots showed that increasing stenosis severity amplified
throat jet velocities and extended recirculation zones, while shoulder length governed the sharpness and spatial extent of disturbed flow. The pulsatile Carreau model revealed systolic acceleration and diastolic deceleration in velocity contour plots, greater pressure drops with stenosis severity. It also showed wall shear stress (WSS) distributions characterised by high shear at stenotic throats and low or oscillatory shear effects downstream. These disturbed, low-WSS regions were identified as potential nanoparticle deposition sites for pharmacodynamics treatments, aligning with prior findings on plaque-prone haemodynamics. The results demonstrate that stenosis severity amplifies haemodynamic disturbances, while
shoulder length shapes their distribution, together influencing the likelihood of nanoparticle residence and deposition. These findings are consistent with published literature, supporting CFD as a predictive tool for assessing hemodynamics. Future research could integrate deformable arterial walls through fluid–structure interaction (FSI), patient-specific geometries, and explicit nanoparticle transport for drug delivery in clinical translation.
