Plaque deposition in human arteries leads to stenosis, a condition that obstructs blood flow and alters the distribution of wall shear stress (WSS), contributing to vascular disease progression. When a bend is present in the artery, hemodynamic disturbances intensify, further exacerbating pathological wall loading. In the present study, pulsatile flow in straight and bent stenosed arterial models have been investigated numerically using ANSYS-Fluent® 18.0 for Reynolds numbers (Re) within 300–1200 and Womersley numbers (Wo) from 7.62 to 15.24. Flow imaging was conducted for $\text{Re}=1200$, $\text{Wo}=7.62$ to validate numerical results. Compared with the straight model, the bent model exhibits stronger shear layers and larger, more coherent three-dimensional (3D) vortical structures, as visualized using the $d_2$-criterion. These vortices disintegrate dynamically during diastole, correlating with higher WSS values ($\approx 42\mathrm{N}/{\mathrm{m}}^2$) near the stenosis in the bent model versus $\approx 37\mathrm{N}/{\mathrm{m}}^2$ in the straight model. Time-averaged wall shear stress (TAWSS) is elevated in the bent model ($\approx 10\mathrm{N}/{\mathrm{m}}^2$ versus $\approx 6\mathrm{N}/{\mathrm{m}}^2$), while the oscillatory shear index (OSI) approaches a value 0.5 downstream, indicating greater exposure to fluctuating loads. The breakdown of 3D vortical structures during diastole is directly linked to enhanced wall loading in the bent model. Overall, the bent geometry amplifies flow disturbances, with dynamic vortex breakdown and extended regions of oscillatory loading, making it more susceptible to disease progression. These findings emphasize the critical influence of arterial geometry on flow dynamics and disease progression. The suppression of vortices at a higher pulsation frequency ($\text{Wo}=15.72$) suggests exercise as a preventive measure to stabilize flow, reduce adverse shear stresses, and mitigate risks of vascular disease.

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• Blood flow
• Haemodynamics
• Physiological flows