Multiphysics CFD–FSI–DPM analysis of nanoparticle transport and near-wall retention in carotid artery bifurcations

Understanding the transport and near-wall dynamics of nanoparticles in arterial bifurcations is critical for elucidating atherogenesis and optimising nanotherapeutic design. This study systematically investigated the behaviour of nanoparticles (18–200 nm) in carotid artery bifurcations under physiologically realistic pulsatile conditions, using a coupled CFD–FSI–DPM framework. The influence of particle size, injection site, blood rheology (original and modified Carreau models), arterial wall mechanics (rigid, one-way, and two-way FSI), and endothelial surface roughness was evaluated on key hemodynamic parameters, including Particle Residence Time (PRT), wall shear stress, vorticity, and flow patterns. Boundary-layer injections consistently prolonged particle residence, with small (18 nm) nanoparticles showing high endothelial penetration potential and large (200 nm) particles achieving maximal near-wall retention (∼1.2 %). Localised bifurcation regions further amplified residence times, highlighting the critical role of disturbed near-wall hemodynamics. Vessel compliance enhanced near-wall trapping, with two-way FSI predicting peak arterial displacements (∼1.43 mm) and Von Mises stresses (∼0.04 MPa), while one-way FSI nearly doubled particle residence compared with rigid-wall models. The modified Carreau model maintained higher viscosity in low-shear regions, producing broader wall shear stress distributions (∼19 Pa) and smoother flow, which prolonged early particle retention (∼4.46 % at 0.5 s). Surface roughness amplified retention, physiological (∼1.1 µm) and pathological (∼10 µm) roughness promoting particle accumulation (∼7.6–9.8 %). Overall, nanoparticle transport in bifurcating arterial flows is governed by the coupled effects of flow unsteadiness, vascular mechanics, non-Newtonian rheology, particle size, injection strategy, and wall microtopography. The validated multiphysics platform provides mechanistic insight into LDL entrapment and plaque initiation and offers design-relevant guidance for nanoparticle-based therapeutics and patient-specific analyses.