Cardiovascular prevention in childhood and young adults

Cardiovascular prevention begins long before adulthood. Increasing evidence demonstrates that cardiovascular risk trajectories are established early in life, shaped by inherited susceptibility, foetal and then environmental exposures, psychosocial burden, and cardiometabolic profiles that frequently persist into adulthood. This issue of the European Journal of Preventive Cardiology highlights the concept that primordial and primary prevention should be considered a life-course continuum, extending from prenatal development through childhood, adolescence, and young adulthood. Familial hypercholesterolaemia (FH) represents one of the clearest examples of how early cardiovascular risk may be modified through timely intervention. In the study entitled ‘Effectiveness and safety of treatment for heterozygous familial hypercholesterolaemia and multifactorial dyslipidaemia in children: an overview of systematic reviews’, Le Thi et al.1 from Germany demonstrate that statins remain the cornerstone of treatment for paediatric FH, with newer lipid-lowering therapies, including PCSK9 inhibitors, providing substantial reductions in LDL cholesterol (LDL-C), although with limited long-term safety data. Complementing these findings, in ‘Evolocumab treatment reduces carotid intima-media thickness in paediatric patients with heterozygous familial hypercholesterolaemia’, Wiegman et al.2 from the Netherlands show that evolocumab not only reduced LDL-C but also improved carotid intima-media thickness among children receiving background statin therapy, suggesting that early intervention may favourably alter vascular trajectories before irreversible atherosclerotic changes develop. Together, these findings support the concept that timely lipid-lowering intervention during childhood may substantially modify lifelong cardiovascular risk. Early cardiovascular risk identification remains equally important. In ‘Proposal of a familial hypercholesterolemia paediatric diagnostic score (FH-PeDS)’, Kafol et al.3 from Slovenia and Portugal developed novel paediatric diagnostic models outperforming traditional FH criteria and improving recognition of genetically confirmed disease. Likewise, lipid-related cardiovascular risk extends beyond LDL-C (Figure 1). In ‘The association of childhood HDL cholesterol with atherosclerotic cardiovascular disease events in adults’, Wang et al.4 from Australia report the persistent low childhood HDL cholesterol is associated with increased adult atherosclerotic cardiovascular disease risk. Collectively, these studies emphasize that effective prevention of premature cardiovascular disease in FH requires an integrated pathway of early diagnosis, risk stratification, and treatment initiation during childhood. Familial hypercholesterolemia paediatric diagnostic score, reproduced from Kafol et al.3 The transition from adolescence to adulthood appears to represent another critical window for cardiovascular prevention. In ‘The contribution of adolescent cardiovascular disease risk factors to vascular stiffness and cardiac remodelling in young adults’, Barden et al.5 from Australia demonstrate that adolescents with clustered cardiovascular risk factors exhibited greater pulse wave velocity, increased left ventricular mass, and impaired myocardial function at 27 years of age, independent of contemporary cardiovascular risk profiles. These findings reinforce the concept that vascular and cardiac remodelling may already be established in early adulthood. Similarly, obesity-related remodelling may emerge silently in otherwise healthy individuals. In ‘Association of epicardial adipose tissue thickness and cardiac structure and function in early midlife: the cardiovascular risk in Young Finns Study’, Gustafsson et al.6 from Finland reported independent associations between epicardial adipose tissue and increased left ventricular wall thickness, left atrial enlargement, and impaired diastolic relaxation, highlighting a potential imaging biomarker for early cardiovascular risk detection. Weight trajectories throughout childhood and adolescence also appear to exert long-term cardiovascular consequences. In ‘Body mass index during childhood and puberty: associations with blood pressure and hypertension’, Lilja et al.7 from Sweden showed that pubertal body mass index increase independently predicted midlife blood pressure and hypertension in both sexes, while childhood adiposity itself predicted later blood pressure particularly among men. Importantly, much of this association was mediated through adult adiposity, emphasizing the persistence of cardiometabolic risk across the life course. Together, these studies underscore the importance of maintaining healthy weight during childhood and adolescence as a cornerstone of cardiovascular prevention. Cardiovascular health may be shaped by environmental influences beginning even before birth. In ‘Effects of ambient air pollutants and environmental greenness on the incidence of pre-/hypertension in children and adolescents’, Wolters et al.8 from Germany and the IDEFICS/I.Family consortium demonstrate that reductions in particulate matter exposure were associated with lower risks of incident hypertension among children and adolescents, while environmental greenness exerted favourable effects. Extending this concept into prenatal life, Renaers et al.9 from Belgium, in ‘Prenatal particulate air pollution exposure predicts arterial stiffness in childhood’, found that maternal exposure to fine particulate matter during pregnancy, particularly during the second trimester, was associated with increased arterial stiffness among offspring at 9–11 years of age. These observations support the concept of foetal cardiovascular programming and suggest that prevention strategies should increasingly incorporate environmental and public health perspectives. The interaction between prenatal and adult nutritional environments further reinforces the developmental origins of cardiometabolic disease. In ‘Prenatal and postnatal nutritional mismatch, reflected by birth weight and adult body mass index, and cardiometabolic disease risk’, Chen et al.10 from China found in over 250 000 UK Biobank participants that individuals with low birth weight and obesity in adulthood exhibited the highest risks of atherosclerotic cardiovascular disease, hypertension, diabetes, and hyperlipidaemia, further supported through Mendelian randomization analyses. Such observations strengthen the ‘thrifty phenotype’ hypothesis and emphasize that prenatal undernutrition followed by later nutritional excess may amplify cardiometabolic vulnerability. Subclinical atherosclerosis among young adults may also identify particularly high-risk individuals. In ‘Risk profile and prognostic implications of premature advanced coronary atherosclerotic disease among young to early middle-aged adults: the coronary artery calcium consortium’, Boakye et al.11 from the USA demonstrate that advanced coronary artery calcium burden in younger adults was associated with substantially increased cardiovascular and all-cause mortality, underscoring the prognostic relevance of early coronary imaging.8 Interestingly, in ‘Minimal extra-cardiac atherosclerosis present in young people with sudden cardiac death due to coronary artery disease’, Paratz et al.12 from Australia, report that severe coronary disease in younger individuals frequently occurred in the absence of widespread extracardiac atherosclerosis, suggesting that early coronary disease may sometimes represent a more localized rather than systemic process. Not all preventive strategies require sophisticated imaging or biomarkers. In ‘Added predictive value of childhood physical fitness to traditional risk factors for adult cardiovascular disease’, Fraser et al.13 from Australia demonstrated that childhood cardiorespiratory and muscular fitness modestly improved the prediction of adult obesity, metabolic syndrome, and low HDL cholesterol beyond traditional childhood cardiovascular risk factors. Given its feasibility, low cost, and non-invasive nature, childhood physical fitness may represent an underutilized marker of future cardiovascular health and deserves greater consideration in public health surveillance. Finally, cardiovascular prevention in youth must extend beyond biology and behaviour to encompass psychosocial determinants. In ‘Childhood exposure to multiple types of violence and adult cardiovascular disease’, Cui et al.14 from China and the USA report childhood exposure to violence from parents, siblings, or peers being associated with significantly increased risks of adult cardiovascular disease, with depressive symptoms partially mediating these associations (Figure 2). These findings broaden the framework of cardiovascular prevention and highlight the importance of family, school, and mental health interventions in reducing long-term cardiovascular vulnerability. Cumulative hazard of cardiovascular disease according to childhood violence exposure. Cardiovascular disease comprised myocardial infarction, angina, coronary artery disease, heart failure, and other reported cardiac disorders. Childhood violence exposure referred to any history of abuse or bullying by parents, siblings, or peers occurring before 17 years of age, reproduced by Cui et al.14 In summary, the studies presented in this issue reinforce the concept that cardiovascular prevention should no longer be viewed as an adult-centred discipline but rather as a lifelong continuum beginning before birth and extending through childhood, adolescence, and young adulthood. Early recognition of inherited susceptibility, healthier environments, improved physical fitness, psychosocial support, and sustained cardiometabolic risk control may together provide the greatest opportunity to alter cardiovascular trajectories before disease becomes clinically manifest. Victor Aboyans (Writing—review & editing [supporting]), and Panteleimon E. Papakonstantinou (Writing—original draft [lead])