Herz · Nov 5, 2026
Inherited cardiovascular risk and its impact on healthspan and lifespan
By Li L, Schunkert L, Schunkert H
Genetic disposition for cardiovascular disease (CVD) is a major determinant of aging-related traits, such as healthspan, dementia, and frailty. While rare monogenic disorders provide important mechanistic insights, most CVDs and aging-related traits are driven by the cumulative effects of numerous common genetic variants, resulting in a polygenic risk architecture. Analyses of genes and pathways affected by these variants revealed significant correlations in the genetic architectures of CVD and aging, which appear to promote each other bidirectionally. Thus, CVD and aging share common genetic mechanisms, linking inherited cardiovascular risk to frailty, dementia, reduced healthspan, and shortened lifespan—and, conversely, explaining why aging is the strongest risk factor for atherosclerosis. Advances in genome-wide association studies have also enabled the construction of a polygenic risk score (PRS), which quantifies inherited CVD risk and facilitates early risk stratification beyond conventional clinical assessment. Importantly, individuals at high polygenic risk for CVD derive greater benefit from preventive strategies, which reduce their lifelong burden of CVD risk and ultimately promote healthy aging. Therefore, personalizing clinical risk assessment by integrating genetic testing for both CVD and aging-related traits may be of clinical importance. Specifically, lifestyle modification and preventive therapies based not only on conventional risk assessment, but also on polygenic risks may offer an individualized life-course approach for precision prevention, shifting cardiovascular care from reactive disease management toward the promotion of healthy aging.