Increased arterial stiffness, as measured by pulse wave velocity (PWV), is increasingly recognised as an important predictor of future cardiovascular events. At present, the mechanisms leading to arterial stiffening and the processes underlying its association with cardiovascular disease remain unclear. One suggestion is that stiffening may be caused by atherosclerosis along the aorta, explaining its association with atherothrombotic cardiovascular events. However, other than age and blood pressure, there is little or no association between arterial stiffness and established risk factors for atherosclerosis. PWV is not increased in early stages of atherosclerosis, as manifest by intima-media thickening and presence of non-calcified atheromatous plaque, but is associated with presence of calcified plaque and calcification of the aorta. Furthermore, the correlation between PWV and vascular calcification is in the majority explained by common genetic factors. One consequence of increased large artery stiffness is an increase in pulse pressure, which, in older subjects, is the blood pressure components most closely correlated with cardiovascular events. Arterial stiffening increases early aortic pressure generated from ventricular contraction. However, this pressure wave can further be increased by an amount called the augmentation pressure, traditionally attributed to pressure wave reflection, which is associated with arterial tapering independently of PWV. Augmentation pressure is an important contributor to age-related increase in central PP, especially in women <50 years of age, and can be effectively reduced by nitrovasodilation independently of any change in arterial stiffness.