Deformation Driven Hemodynamics in a Compliant Coronary Artery With Serial Stenosis: A Layer-Resolved Fluid-Structure Interaction Study

Coronary artery disease often manifests as serial stenosis in mechanically compliant vessels, where pulsatile flow, wall deformation, and plaque heterogeneity govern hemodynamic behavior. This study develops a two-way fluid-structure interaction (FSI) framework to investigate pulsatile blood flow through a compliant coronary artery with serial stenoses. The arterial wall is modeled using a realistic three-layer representation. The intima, media, adventitia, and fibrous cap are treated as hyperelastic solids, while the encapsulated lipid pool is modeled as a linear elastic inclusion. Blood is represented as a non-Newtonian Carreau fluid to capture shear-dependent rheology under physiological conditions. By systematically varying plaque stiffness and pulsatile inertia, quantified through the Womersley number (Wo), the analysis resolves modulation of lumen dynamics, pressure loss, vortex structure, and near-wall transport. Increasing plaque stiffness suppresses wall deformation, preserves a narrower effective lumen, and intensifies jet acceleration and adverse pressure gradients across interacting lesions. This leads to increased cycleaveraged pressure drop and hemodynamic resistance. Elevated heart rate enhances unsteady inertial effects, strengthens temporal pressure fluctuations, and prolongs post-stenotic vortex persistence, particularly in serial stenosis where upstream flow preconditioning alters downstream dynamics. These effects modify clinically relevant indices such as fractional flow reserve, time-averaged wall shear stress, and wall shear stress divergence, indicating deformation-dependent changes in near-wall convective transport. A forcebased scaling analysis quantifies the relative roles of elastic resistance, pulsatile inertia, and viscous dissipation. The resulting linear collapse of normalized pressure loss provides a mechanistic interpretation of trans-stenotic pressure deficits in compliant, serially stenosed arteries.