Deformation-driven hemodynamics in a compliant coronary artery with serial stenosis: A layer-resolved fluid–structure interaction study

Coronary artery disease manifests as serial stenosis in compliant vessels, where pulsatile flow, wall deformation, and plaque heterogeneity govern hemodynamic behavior. This study develops a two-way fluid–structure interaction framework to investigate blood flow through a compliant coronary artery with serial stenoses. The arterial wall uses a 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. By varying plaque stiffness and pulsatile inertia, quantified through the Womersley number (Wo), the analysis resolves lumen dynamics, pressure loss, vortex structure, and near-wall transport. Increasing plaque stiffness from 100 kPa to 10 MPa suppresses radial wall deformation by approximately 30%–50%, preserves a narrower lumen, and intensifies jet acceleration and adverse pressure gradients across interacting lesions. This increases cycle-averaged pressure drop and hemodynamic resistance by nearly two times. Elevated heart rate, with Wo increasing from 2.49 to 3.04, enhances unsteady inertial effects and raises peak pressure drop by approximately 40%–60%. These effects modify clinical indices, with peak time-averaged wall shear stress increasing by up to ∼50% and fractional flow reserve (FFR) decreasing from approximately 0.83 to 0.60 across the stiffness range. Finally, a force-based scaling analysis quantifies the roles of elastic resistance, pulsatile inertia, and viscous dissipation. The resulting linear collapse of normalized pressure loss provides mechanistic interpretation of trans-stenotic pressure deficits in compliant, serially stenosed coronary arteries.