Cardiac Allograft Vasculopathy (CAV) is one of the main long-term complications after heart transplantation and the most relevant manifestation of chronic graft rejection. The disease is characterized by progressive intimal thickening and concentric narrowing of the coronary lumen, driven by the interaction between immunological, cellular, and hemodynamic phenomena. Specifically, disease onset and progression are led by lymphocyte (LYM) and macrophage (MP) infiltration, subsequent smooth muscle cell (SMC) recruitment and proliferation, with associated extracellular matrix (ECM) deposition, and exposure to altered hemodynamic conditions. Despite the central role of murine models in the study of CAV, the understanding of early mechanisms remains limited by the availability of longitudinal observations and by the difficulty of directly measuring local quantities such as Wall Shear Stress (WSS), immune cell distribution, and geometric remodeling.