Aortic stiffness, impaired fasting glucose, and aging.

The arterial wall is subject to a continuous process of structural, cellular, and molecular modifications that involve cellular growth processes, apoptosis, cell migration, inflammation, and fibrosis, resulting in changes of wall structure and dimension, as well as contractile and elastic properties. Physiological remodeling is an adaptive response to hemodynamic changes in the sense of repair or adjustment. Cardiovascular (CV) diseases, such as diabetes mellitus (DM) and hypertension, as well as aging, lead to enhancement of vascular maladaptive processes and the formation of atherosclerotic lesions and calcifications. One essential consequence of these maladaptive processes is the change of the arterial wall structure and the loss of the elastic properties of the conduit arteries, which is of growing clinical relevance. This phenomenon is termed “arterial stiffening.” This process leads to increased pulse wave velocities and an increase of systolic and pulse pressures attributable to an alteration in the timing of reflected waves.1 Various studies using a variety of indices have established that arterial stiffness is increased with CV risk factors for atherosclerosis, is higher in women, and increases with age even in the absence of vascular disease or risk factors.2,3 Elevated blood pressure related to peripheral vasoconstriction increases aortic stiffness, which is an independent predictor of primary coronary events in patients with essential hypertension.4,5 The relevance of arterial stiffness, carotid pulse pressure, and augmentation index, as independent predictors for CV events, comes from epidemiological studies. The largest amount of evidence has been given for aortic stiffness, measured through carotid-femoral pulse wave velocity (PWV), as 10 000 subjects have been included in studies.1