Abstract
Atherosclerosis is a pathological condition associated with arterial narrowing. Altered hemodynamics within stenosed arteries plays a substantive role in myocardial infarction, a medical condition that incorporates high mortality rates. Pulsatile flow hemodynamics (Reynolds number, Re = 200-800, Womersley number, Wo = 5.7-8.1) within asymmetric multiple stenosed vessels is explored. Ventricular pumping initiates a primary vortex nestled in the concavity of stenosis, while at peak systole, wall vorticity unfolds a secondary vortex of opposing sense on either wall. Cycle diastole then unveils a tertiary vortex; however, retrograde flow weakens free shear layers segregating these vortices into newer structures, promoting flow impediment. Spatio-temporal evolution of vortices influencing the disease is then established. Consequently, within the Lagrangian framework evolution of massless tracers injected inflow is correlated to d(2) - criterion and power spectra. Vortex size and strength increase with Re = 200-800 and stenosis severity 50-75%, while they diminish with intensified activity, Wo = 5.7-8.1. Additional harmonics divulging low energies within the power spectra considerably influence particle residence index (PRI). Results reveal that, in an asymmetric 50% occluded artery, atherosclerosis is promoted for Re < 500, while it is suppressed for 500 < Re < 800, respectively. Furthermore, a 75% severity exhibits reduced flow in conjunction with substantial oscillations in signatures of time-averaged wall shear stress (TAWSS) and oscillatory shear index (OSI ~ 0.5), promoting plaque fissure (Re = 800). Interestingly, these triggering events are likewise revealed in a 50% occluded artery manifesting secondary stenosis at Re = 800.