Arterial stiffness and atherosclerosis: mechanistic and pathophysiologic interactions

There are significant mechanistic and pathophysiologic interactions between arterial stiffness, atherosclerosis, and hemodynamic stress. Atherosclerosis is triggered by endothelial cell dysfunction. Subsequent lipid accumulation and increased inflammation facilitate the formation of pathological vulnerable plaques. This results in the development of atherosclerotic cardiovascular disease. In contrast, arterial stiffness results from elastin breakdown, wall calcification, fibrosis, collagen, and elastin cross-linking, increased vascular smooth muscle cell tone, and endothelial cell dysfunction. Both these types of vascular failure share pathophysiological mechanisms, involving aging, inflammation, and metabolic and hemodynamic risk factors. In addition, both are important contributors to cardiovascular risk. The systemic hemodynamic atherosclerotic syndrome has been proposed as a novel clinical entity linking arterial stiffness, atherosclerosis, and hemodynamic stress, ultimately contributing to target organ damage and cardiovascular events.