Cardiac Allograft Vasculopathy (CAV) is a leading cause of chronic graft rejection in heart transplant (HTx) recipients, with an incidence of 50% within 10 years post-HTx and an associated 30% mortality rate. CAV is characterized by progressive intimal thickening and luminal narrowing of the coronary arteries. Its multiscale nature is reflected in the interplay between immunological (e.g., lymphocyte (LYM) and macrophage (MP) infiltration), biomechanical (e.g., disturbed flow patterns like low wall shear stress (WSS)), and geometrical (e.g., irregular arterial wall shape profiles) factors. Current therapies are limited, with re-transplantation being the only definitive solution. Moreover, diagnosis remains challenging and typically possible only at late stages, due to an incomplete understanding of the mechanisms underlying the disease early onset.