title: Influence of age, risk factors, and cardiovascular and renal disease on arterial stiffness: clinical applications.
abstract: Age is the main clinical determinant of large artery stiffness. Central arteries stiffen progressively with age, whereas peripheral muscular arteries change little with age. A number of clinical studies have analyzed the effects of age on aortic stiffness. Increase of central artery stiffness with age is responsible for earlier wave reflections and changes in pressure wave contours. The stiffening of aorta and other central arteries is a potential risk factor for increased cardiovascular morbidity and mortality. Arterial stiffening with aging is accompanied by an elevation in systolic blood pressure (BP) and pulse pressure (PP). Although arterial stiffening with age is a common situation, it has now been confirmed that older subjects with increased arterial stiffness and elevated PP have higher cardiovascular morbidity and mortality. Increase in aortic stiffness with age occurs gradually and continuously, similarly for men and women. Cross-sectional studies have shown that aortic and carotid stiffness (evaluated by the pulse wave velocity) increase with age by approximately 10% to 15% during a period of 10 years. Women always have 5% to 10% lower stiffness than men of the same age. Although large artery stiffness increases with age independently of the presence of cardiovascular risk factors or other associated conditions, the extent of this increase may depend on several environmental or genetic factors. Hypertension may increase arterial stiffness, especially in older subjects. Among other cardiovascular risk factors, diabetes type 1 and 2 accelerates arterial stiffness, whereas the role of dyslipidemia and tobacco smoking is unclear. Arterial stiffness is also present in several cardiovascular and renal diseases. Patients with heart failure, end stage renal disease, and those with atherosclerotic lesions often develop central artery stiffness. Decreased carotid distensibility, increased arterial thickness, and presence of calcifications and plaques often coexist in the same subject. However, relationships between these three alterations of the arterial wall remain to be explored.
authors.affiliation: IPC Center, Paris, France. benetos@ccr.jussieu.fr
authors.forename: Athanase
authors.initials: A
authors.lastname: Benetos
authors.forename: Bernard
authors.initials: B
authors.lastname: Waeber
authors.forename: Joseph
authors.initials: J
authors.lastname: Izzo
authors.forename: Gary
authors.initials: G
authors.lastname: Mitchell
authors.forename: Lawrence
authors.initials: L
authors.lastname: Resnick
authors.forename: Roland
authors.initials: R
authors.lastname: Asmar
authors.forename: Michel
authors.initials: M
authors.lastname: Safar
mesh_terms: D000375:Aging / Q000502:physiology*; D001011:Aorta / Q000503:physiopathology; D001161:Arteriosclerosis / Q000503:physiopathology*; D003327:Coronary Disease / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000503:physiopathology*; D012307:Risk Factors; D014655:Vascular Resistance / Q000502:physiology*