Finite volume incompressible lattice Boltzmann method simulation of pulsatile blood flow in arteries with multiple stenosis: A hemodynamic analysis

Atherosclerosis remains a leading cause of cardiovascular mortality, with multi-stenotic arteries posing critical hemodynamic challenges due to amplified shear stress patterns and flow disturbances. The present study investigates how stenosis severity, stenosis configuration, and pulsatile flow parameters (Reynolds/Womersley numbers) alter shear stress indices-time-averaged wall shear stress (TAWSS) and oscillatory shear index (OSI) alongside cross-sectional indices reverse flow fraction (RFF) and fractional flow reserve (FFR). Using the finite volume incompressible lattice Boltzmann method (FV-iLBM) framework, pulsatile non-Newtonian blood flow through sequential stenoses is simulated. The FV-iLBM framework resolves physiologically relevant pulsatile flow, eliminating conventional pressure solvers, and preserving exact mass conservation in complex geometries while capturing shear-rate-adaptive viscosity using the Carreau model. Results indicate that elevated Reynolds and Womersley numbers amplify inertial effects and flow pulsatility, intensifying pressure gradients and oscillatory flow downstream of stenoses. At higher Reynolds numbers, steeper near-wall velocity gradients intensify wall shear stress and amplify mean pressure drops across stenoses, thereby exacerbating endothelial dysfunction, whereas elevated Womersley numbers accentuate transient flow separation and induce pronounced pressure fluctuations. Across stenosis configurations, the location of the largest stenosis markedly alters pressure distribution and shear stress patterns, especially when placed upstream of smaller lesions. For instance, configurations with the large stenosis downstream exhibit a 56% reduction in peak wall shear stress at the throat, while upstream positioning promotes elevated OSI in distal regions—both linked to disturbed flow and heightened endothelial risk. These findings emphasize incorporating patient-specific hemodynamics, as local flow unsteadiness and inertia may critically affect disease progression.