Fig. 1: Relative contribution of structural and functional complications in preterm cardiovascular disease risk across the lifespan.

Structural impairments (e.g., altered cardiac geometry^38,146, ↓ microvascular density^76,77) incurred with preterm birth ( < 37 weeks’ gestation) outside of clinically significant ones (e.g., patent ductus arteriosus) contribute relatively little to cardiovascular dysfunction, whereas functional complications (inotrope insensitivity⁷¹, ↑ microvascular perfusion⁶²) are a significant cause of dysfunction (e.g., pulmonary hypertension^96,147,148, ↓ cardiac output^70,71). Surviving graduates of neonatal intensive care exhibit little cardiovascular dysfunction following discharge and throughout infancy. By childhood, structural limitations from prematurity become apparent (↓ LV mass⁹⁴, ↑ RV mass⁹⁵), resulting in some (dys)functional changes (↓ contractility^94,95, ↑ BP^90,93,145). Persistent structural limitations (altered cardiac geometry^55,57,119, ↓ arterial diameter, ↓ microvascular density) contribute to cardiovascular remodelling (concentric hypertrophy^57,112,134) and dysfunction in early adulthood (cardiac fibrosis^58,134, arterial stiffness^111,149, ↑ BP²⁸). In combination with ‘traditional’ cardiovascular disease risk factors, these preterm-specific risk factors fuel the onset of disease.