High-fidelity simulations are conducted to analyze physiological flows in non-planar curved artery models using physiological flow rates under pulsatile flow conditions. Additional simulations are performed under steady flow conditions at various Reynolds numbers, as well as for planar curved models for comparison. The results indicate that the torsion-induced effects are more pronounced under pulsatile flow than in steady conditions. During the acceleration phase, streamwise velocity peaks near the outer-upper wall close to the inlet and gradually shifts toward the outer-lower wall downstream, reinforcing asymmetric centrifugal effects. As flow transitions to deceleration, the streamwise velocity weakens, but the secondary flows intensify, further highlighting the influence of torsion. These asymmetric secondary flows lead to pronounced differences between the upper and lower deformed Dean (DD) vortices, with the lower DD vortex typically becoming larger and more persistent. Torsion also alters the trajectory and strength of deformed Lyne (DL) and split-Dean (SD) vortices, resulting in earlier vortex splitting and more complex interactions along the pipe, including asymmetric merging between upper and lower structures. Furthermore, torsion alters the wall shear stress (WSS) patterns, leading to asymmetric WSS distributions with localized regions of elevated and reduced WSS on the upper and lower walls, along with high oscillatory behavior throughout the cardiac cycle.
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