Cardiac allograft vasculopathy (CAV) is a major cause of heart transplant rejection. CAV is an accelerated form of coronary artery disease that affects the allograft. It is characterized by progressive intimal thickening due to a complex interplay between immunological and non-immunological events. The underlying mechanisms of CAV are largely unknown. To gain a better knowledge of its dynamics, many pre-clinical studies (e.g., in vivo models) are needed, but they are often associated with high costs, long protocol timelines and ethical concerns. Moreover, access to crucial time points across the experimental follow-up and measurements of biomechanical quantities are critically difficult. Consequently, the use of in vivo models remains somehow constrained, fostering the research to exploit alternative methodologies.