Vascular age

Vascular age is a clinical concept and physiological metric that estimates the biological state of an individual's cardiovascular system relative to their chronological age. It is not a single molecular target or receptor but rather a composite phenotypic expression of arterial health, primarily determined by measurable parameters like arterial stiffness, endothelial function, and atherosclerotic burden [1, 14]. The concept was popularized by the Framingham Heart Study to improve cardiovascular risk communication, translating complex risk profiles into an intuitive 'age' to motivate patient lifestyle changes and treatment adherence [3, 11]. Pathologically, advanced vascular age involves the degradation of elastin fibers, increased collagen cross-linking, and the accumulation of vascular senescent cells, leading to increased pulse wave velocity and systolic blood pressure [2, 5]. While no direct 'vascular age' ligands exist, therapeutic interventions such as statins, ACE inhibitors, and SGLT2 inhibitors can mitigate or reverse the signs of vascular aging by acting on specific molecular pathways like HMG-CoA reductase or the renin-angiotensin system [6, 10, 12]. Monitoring this concept involves non-invasive biomarkers, most notably carotid-femoral pulse wave velocity (cfPWV), which serves as the gold standard for assessing arterial stiffness [9, 15].

Other names

Heart ageArterial ageBiological vascular ageEarly vascular aging (EVA)

Drugs do not target 'vascular age' directly as it is not a specific molecule; however, they improve this clinical metric by inhibiting HMG-CoA reductase (statins), blocking the renin-angiotensin-aldosterone system (ACE inhibitors and ARBs), or activating longevity pathways such as SIRT1 to reduce arterial stiffness, inflammation, and oxidative stress.