The arterial–venous continuum: bridging atherosclerosis and chronic venous disease through endothelial dysfunction

Atherosclerosis and chronic venous disease are among the most common vascular disorders worldwide and frequently coexist in the same individuals. Although traditionally regarded as distinct entities-one arterial and lipid-driven, and the other venous and pressure-related-emerging evidence suggests that they may share systemic determinants and overlapping biological pathways. This narrative review examines epidemiological and mechanistic evidence supporting potential links between atherosclerosis and chronic venous disease, and discusses implications for integrated vascular risk assessment. Observational studies report associations between the presence and clinical severity of chronic venous disease and a higher prevalence of atherosclerotic cardiovascular disease, peripheral artery disease, cerebrovascular disease, and increased all-cause mortality. Mechanistic research identifies converging processes-including systemic inflammation, oxidative stress, reduced nitric oxide bioavailability, extracellular matrix remodeling, and endothelial dysfunction-that affect both arterial and venous territories. Hemodynamic interactions between the arterial and venous systems may contribute to microvascular dysfunction and tissue hypoxia. Large-scale population analyses have also described associations between varicose veins and cognitive decline, including vascular dementia; however, these findings derive from observational data and do not establish causality. The concept of an arterial-venous continuum provides a biologically plausible and hypothesis-generating framework for understanding shared vascular vulnerability. Nevertheless, current evidence remains predominantly observational, and chronic venous disease should be regarded primarily as a potential marker of systemic endothelial dysfunction rather than a proven causal mediator of atherosclerotic progression. Further longitudinal and interventional studies are needed to clarify directionality and determine whether treatment of venous disease influences arterial outcomes.