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Preterm birth has evolved from being an acute neonatal challenge to a lifelong health determinant, as advances in neonatal care have markedly improved the survival of very and extremely preterm infants. This narrative review synthesizes epidemiological and mechanistic evidence linking preterm birth with heightened cardiometabolic risk across the life course. In adulthood, individuals born preterm demonstrate increased rates of heart failure, ischemic heart disease, stroke, atrial fibrillation, and diabetes. Beneath these overt clinical outcomes lies a distinct phenotype characterized by increased adiposity, insulin resistance, dyslipidemia, hypertension, and atypical growth trajectories, with rapid catch-up growth amplifying long-term risk. Mechanistic pathways highlight adipose tissue maldevelopment, predisposing to metabolic syndrome, alongside cardiac maldevelopment with reduced ventricular size, impaired diastolic function, and diminished exercise capacity. Furthermore, vascular growth arrest, impaired elastin synthesis, and nephron deficiency contribute to sustained elevations in blood pressure, establishing an early substrate for hypertension and cardiovascular remodeling. These alterations reflect the developmental origins of health and disease, whereby early-life disruption of growth and maturation exerts lasting effects on organ structure and function. Collectively, the evidence identifies adults born preterm as a growing yet under-recognized patient population with a unique clinical and biochemical profile and accelerated vulnerability to non-communicable diseases. Greater awareness among pediatric and adult physicians, structured transition of care, and targeted prevention strategies are urgently needed to mitigate early cardiometabolic morbidity and optimize long-term health outcomes in this high-risk group.
Ficial et al. (Mon,) studied this question.