Abstract
Abstract The aetiology of preterm cardiovascular disease formation appears different from that of traditional population. Within the ‘traditional’ population cardiovascular disease formation is driven by functional stressors (e.g., diet, smoking). Whereas preterm cardiovascular disease risk is driven by structural changes incurred at birth. Much of the proliferative growth in the developing heart and major vessels ceases at birth, leading to permanently reduced dimensions compared to their term-born cohort. These structural changes take a back seat to functional and clinical complications within the neonatal period, but become increasingly pronounced from adolescence, at which point functional decompensation can be observed. While the cause may differ from ‘traditional’ populations, the eventual disease outcomes do not, leading them to be an overlooked population. This means that aetiology, and thus, treatment options may be very different due to the underlying mechanisms. Here, we propose that the structural cause of preterm-associated cardiovascular disease is apparent and observable early in life. Understanding the differences in cardiovascular disease aetiology may therefore aid in the early treatment of preterm-associated cardiovascular disease risk.