Erick Eduardo López Santos

Cardiovascular multimorbidity in young adults is an increasingly relevant clinical and public health concern because multiple cardiovascular, metabolic, renal, behavioral, and psychosocial risk factors may coexist long before overt cardiovascular disease becomes clinically evident. This study analyzed the emerging burden of cardiovascular multimorbidity in young adults, emphasizing conventional and emerging risk factors, early detection strategies, and population-level consequences. An integrative literature review was conducted using recent epidemiological studies, prospective cohorts, systematic reviews, scientific statements, and contemporary cardiovascular risk frameworks. The evidence showed that obesity, dyslipidemia, hypertension, impaired glucose metabolism, nicotine exposure, physical inactivity, poor sleep, and psychosocial factors frequently cluster during early adulthood. Additional markers such as apolipoprotein B, lipoprotein(a), renal dysfunction, central adiposity, and cumulative low-density lipoprotein cholesterol exposure may provide complementary information regarding long-term cardiovascular vulnerability. The findings also demonstrated that short-term cardiovascular risk estimates may underestimate the lifetime impact of prolonged exposure to multiple risk factors in younger individuals. Early detection therefore requires a multidimensional approach integrating clinical, anthropometric, laboratory, behavioral, familial, and social information. From a population perspective, the early onset of multimorbidity may increase future cardiovascular events, chronic healthcare utilization, premature disability, and economic burden. A life-course approach to cardiovascular prevention, focused on early recognition and reduction of cumulative risk exposure, may improve long-term cardiovascular health and limit progression toward established cardiovascular disease.

Cardiovascular disease remains the leading cause of mortality worldwide, despite significant advances in prevention and treatment strategies. Increasing evidence indicates that traditional risk factors alone are insufficient to fully explain cardiovascular risk, highlighting the importance of inflammatory and metabolic mechanisms in the development and progression of atherosclerotic disease. This review synthesizes current scientific evidence on the role of chronic low-grade inflammation and metabolic dysregulation as interconnected determinants of cardiovascular risk. The analysis integrates mechanistic, clinical, and population-level data describing how immune activation, insulin resistance, obesity, metabolic syndrome, and endothelial dysfunction interact to promote atherosclerosis and related cardiovascular outcomes. Particular attention is given to inflammatory signaling pathways, immune cell involvement, and the concept of residual inflammatory risk, which persists even in the presence of optimal lipid control. Additionally, the review examines the contribution of lifestyle factors as upstream modulators of immunometabolic processes. By adopting an integrative immunometabolic perspective, this review provides a comprehensive framework for understanding cardiovascular risk beyond conventional models. This approach is especially relevant for educational and clinical contexts in regions undergoing epidemiological transition, including Mexico, Colombia, and Ecuador. The findings support the incorporation of inflammatory and metabolic determinants into cardiovascular risk assessment, prevention strategies, and future research agendas.

Cardiovascular disease remains the leading cause of global morbidity and mortality, despite significant advances in lipid management and risk factor control. Emerging evidence indicates that cardiometabolic dysfunction and chronic low-grade inflammation act synergistically to accelerate early vascular injury long before the onset of overt clinical events. This review integrates contemporary epidemiological data, mechanistic insights, biomarker analyses, and randomized clinical trial evidence to examine the cardiometabolic–inflammatory–vascular axis as a unified framework for early cardiovascular risk assessment. Population-level data confirm the sustained global expansion of cardiovascular burden, paralleled by increasing prevalence of metabolic syndrome and insulin resistance. Inflammatory biomarkers such as high-sensitivity C-reactive protein and interleukin-6 demonstrate graded associations with incident cardiovascular events, independent of traditional risk factors. Arterial stiffness emerges as a measurable intermediate phenotype reflecting cumulative metabolic and inflammatory exposure, with higher quartiles associated with substantially increased event rates. Furthermore, randomized trials targeting inflammatory pathways show reductions in major adverse cardiovascular events in selected high-risk populations, supporting inflammation as a modifiable contributor to atherosclerotic progression. The integration of inflammatory biomarkers into traditional prediction models yields modest but consistent improvements in discrimination and risk stratification. These findings collectively support a paradigm shift toward earlier biological detection of vascular dysfunction. Such an approach is particularly relevant for regions experiencing rapid growth in cardiometabolic risk, including Mexico, Colombia, and Ecuador. Advancing cardiovascular prevention will require integrative strategies that combine metabolic control, inflammatory assessment, and early vascular evaluation within a precision-based framework.