Hemodynamics in a stenosed artery considering blood viscoelasticity and flow pulsatility

Arterial stenosis poses a serious cardiovascular threat, one that becomes more critical during exercise when an elevated heart rate amplifies wall shear stress at the narrowed section of the artery. This increased stress leads to plaque rupture and clot formation, raising the risk of stroke and further weakening the artery's health. Thus, understanding the complex hemodynamics in diseased arteries is essential for assessing key hemodynamic parameters that guide risk assessment and the development of effective treatment strategies. A primary challenge in achieving this is accurately capturing blood rheology-whether through analog fluids or mathematical models. Many studies simplify blood behavior by assuming it to be either Newtonian or purely shear-thinning, often overlooking its viscoelastic nature. This simplification is problematic in pathological conditions like diabetes mellitus, where increased red blood cell aggregation enhances blood elasticity, requiring a viscoelastic model for accurate hemodynamic analysis. The present study examines the effects of blood viscoelasticity and flow pulsatility on hemodynamics in a 75% stenosed artery under exercise conditions, using waveforms with pulsatility indices of 0.958, 1.126, and 1.373, all at a fixed Womersley number. These effects are evaluated by comparing the results from the multimode simplified Phan-Thien–Tanner (sPTT) and multimode Giesekus models with those from the Newtonian and Carreau–Yasuda models. Our findings reveal that incorporating the viscoelastic properties of blood results in the concentration of vortex centers near the distal end of the stenosis. This localized clustering of vortex centers facilitates stenosis progression. Additionally, as the pulsatility index rises, the differences in time-averaged wall shear stress and wall pressure between the viscoelastic and Newtonian models diminish.