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.

Analysis of renin-angiotensin-aldosterone system gene polymorphisms in resistant hypertension

“…The present results support previous clinical and epidemiological studies which prove that a sedentary life style, physical inactivity, smoking, dyslipidemia, and alcohol and sodium intake are also external factors influencing the development of hypertension (31)(32)(33).…”

The effect of a rapid weight loss induced by laparoscopic adjustable gastric banding on arterial stiffness, metabolic and inflammatory parameters in patients with morbid obesity

“…16 Numerous cardiovascular risk factors, including diabetes, hypertension, hyperlipidemia, cigarette smoking and increasing adiposity, are also associated with increased arterial stiffness, often referred as 'premature arterial stiffening'. [20][21][22] The effect of adiposity on arterial stiffness may begin during childhood and affect the vascular system at a very early stage of vascular aging. 23 Several pre-existing risk factors, including diabetes, hypertension and dyslipidemia, may particularly increase the negative cardiovascular effects of elevated adiposity, causing greater CVD risk at an earlier age in adulthood.…”

Effect of 4 weeks of aerobic or resistance exercise training on arterial stiffness, blood flow and blood pressure in pre- and stage-1 hypertensives

“…12 These changes may be further exacerbated by hypertension. 16,17 Studies investigating flow-mediated vasodilation (FMD) have shown that moderate-intensity AE significantly increased FMD in hypertensive and normotensive subjects, likely mediated through augmented endothelial function. 18,19 There is also evidence that combined AE and RE training programs can improve endothelial function; 20 however, there is only one recent study that has shown an attenuated response to resistance forearm training in a cohort of hypertensive subjects, yet their results may have been confounded with the protocol acceptance of BP medications.…”