The incidence of stent late restenosis is high (Zwart et al., 2010, “Coronary Stent Thrombosis in the Current Era: Challenges and Opportunities for Treatment,” Curr. Treat. Options Cardiovasc. Med., **12**(1), pp. 46–57) despite the extensive use of stents, and is most prevalent at the proximal and distal ends of the stent. Elastic modulus change in stented coronary arteries subject to the motion of the myocardium is not studied extensively. It is our objective to understand and reveal the mechanism by which changes in elastic modulus and geometry contribute to the generation of nonphysiological wall shear stress (WSS). Such adverse hemodynamic conditions could have an effect on the onset of restenosis. Three-dimensional (3D), spatiotemporally resolved computational fluid dynamics (CFD) simulations of pulsatile flow with moving wall boundaries and fluid structure interaction (FSI) were carried out for a helical artery with physiologically relevant flow parameters. To study the effect of coronary artery (CA) geometry change on stent elastic modulus mismatch, models where the curvature, torsion and both curvature and torsion change were examined. The elastic modulus is increased by a factor of two, five, and ten in the stented section for all three modes of motion. The changes in elastic modulus and arterial geometry cause critical variations in the local pressure and velocity gradients and secondary flow patterns. The pressure gradient change is 47%, with respect to the unstented baseline when the elastic modulus is increased to 10. The corresponding WSS change is 15.4%. We demonstrate that these changes are attributed to the production of vorticity (vorticity flux) caused by the wall movement and elastic modulus discontinuity. The changes in curvature dominate torsion changes in terms of the effects to local hemodynamics. The elastic modulus discontinuities along with the dynamic change in geometry affected the secondary flow patterns and vorticity flux, which in turn affects the WSS.