Arterial stiffness is the most important cause of increasing systolic and pulse pressure, and for decreasing diastolic pressure with ageing. Many measures can be applied to quantify arterial stiffness, but all are approximations only, on account of the nonhomogenous structure of the arterial wall, its variability in different locations, at different levels of distending pressure, and with changes in smooth muscle tone. This article summarizes those indices with a focus on newer non-invasive methods and provides an overview of physiological, pathological and pharmacological influences on arterial hemodynamics. In the near future, the ability to detect and monitor subclinical arterial damage will improve cardiovascular risk stratification and act as a better guide in assessing the efficacy of therapeutic interventions than monitoring blood pressure alone. However, large-scale clinical trials are needed to prove the hypothesis that treatment of these new therapeutic targets will translate into clinical benefit, expressed in cardiovascular events or even mortality.