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Some mechanical aspects of arterial aging: physiological overview based on pulse wave analysis

Department of Blood Pressure Research, Tohoku University Graduate School of Medicine, Seiryo-cho, Aoba-ku, Sendai 980-8574, Japan,jhashimoto{at}mail.tains.tohoku.ac.jp

Sadayoshi Ito

Division of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Seiryo-cho, Aoba-ku, Sendai 980-8574, Japan

Aging has a striking impact on the arterial structure and function. The principal structural change with age is medial degeneration that leads to a progressive stiffening of the large elastic arteries. Large artery stiffening increases aortic systolic and pulse pressures through an increase in the forward incident wave and an early return of the backward reflected wave. Peripheral muscular arteries/arterioles are only minimally affected in structure by aging itself, but impaired vasomotor function can alter their impedance properties and thereby increase reflection magnitude. An augmented aortic pressure due to enhanced wave reflection increases wasted left ventricular effort and causes cardiac hypertrophy. Increased pulsatile pressure and flow stresses extend to the vulnerable microcirculation of vasodilated organs such as the brain and kidneys, and can predispose to cerebral lacunar infarction and albuminuria. Although most currently available vasodilators appear to have little direct effect on degenerated elastic arteries, they can act instead on less-degenerated muscular arteries to markedly reduce peripheral wave reflection magnitude and central aortic pressure, and thus contribute to the regression of left ventricular hypertrophy. Further studies are necessary to examine whether the effect of vasodilator therapy on reducing wave reflection contributes similarly to the prevention of microvascular damage in the brain and kidneys.

Key Words: aging • arteriosclerosis • wave reflection • blood pressure • hypertrophy • microcirculation • pulse • pharmacology

This version was published on October 1, 2009

Therapeutic Advances in Cardiovascular Disease, Vol. 3, No. 5, 367-378 (2009)
DOI: 10.1177/1753944709338942


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