Risk Factors for Early Vascular Ageing: A Review of Current Evidence

Abstract

Early vascular ageing (EVA) has become an increasingly important concept in cardiovascular medicine, representing a state in which structural and functional changes of the arterial system occur at a younger age than expected. Unlike chronological ageing, which follows a predictable biological course, EVA reflects an acceleration of vascular decline that predisposes individuals to premature cardiovascular events, stroke, and increased mortality. The central hallmarks of EVA include arterial stiffening, endothelial dysfunction, intima-media thickening, and extracellular matrix remodeling. These alterations are strongly linked to both traditional and emerging cardiovascular risk factors.

This review aims to provide a comprehensive synthesis of current evidence regarding the major determinants of EVA. A structured search of PubMed, Scopus, and Web of Science databases identified epidemiological, clinical, and mechanistic studies published between 2000 and 2024. The findings indicate that non-modifiable risk factors such as age, sex, and genetic predisposition establish the baseline susceptibility to vascular ageing, but modifiable factors play the dominant role in determining the speed and severity of progression. Hypertension, diabetes mellitus, obesity, dyslipidemia, and smoking consistently emerge as the strongest drivers of EVA. Lifestyle-related influences, including sedentary behavior, poor dietary habits, and chronic psychosocial stress, also play significant roles. Moreover, novel contributors such as exposure to environmental pollutants and gut microbiota dysbiosis have been increasingly implicated, expanding the scope of EVA research beyond traditional cardiovascular medicine.

Importantly, the evidence demonstrates that EVA is not irreversible. Lifestyle modification, including regular physical activity, adherence to cardioprotective diets, and smoking cessation, improves arterial elasticity and endothelial function. Pharmacological interventions such as antihypertensive, lipid-lowering, and antidiabetic agents have also been shown to mitigate or delay the onset of EVA. Novel therapeutic approaches targeting oxidative stress, chronic inflammation, and endothelial repair are currently under investigation and may further enhance prevention.

In conclusion, EVA should be recognized as a clinically relevant and potentially preventable condition. Early identification of individuals at risk, integration of vascular ageing markers such as pulse wave velocity into cardiovascular risk assessment, and timely implementation of preventive strategies are essential to reduce the burden of premature cardiovascular disease. By reframing vascular ageing as a modifiable rather than an inevitable process, healthcare systems can shift focus from late-stage treatment to proactive prevention, ultimately improving population health and longevity.