Effect of Age on Pulse Wave Velocity and "Aortic Ejection Time" in Healthy Men and in Men with Coronary Artery Disease

Simonson, Ernst; Nakagawa, K.

doi:10.1161/01.cir.22.1.126

Cited by 64 publications

(35 citation statements)

References 4 publications

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“…Reduced arterial compliance in nonoccluded arteries has been demonstrated in patients with peripheral arterial disease 4 and in patients with coronary artery disease. 7 However, it cannot be stated whether reduced compliance in humans results from atherosclerosis, medial sclerosis, 11 or even from changes such as glycosylation of proteins in the arterial wall. 12 There were 39 subjects, but not all 39 had all observations; thus partial correlation analysis calculations were based on correlations among the same number of variables.…”

Section: Discussionmentioning

confidence: 99%

Risk factors for changes in aorto-iliac arterial compliance in healthy men.

Relf¹,

Lo²,

Myers³

et al. 1986

Arteriosclerosis

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Doppier ultrasound was used to measure pulse wave velocity down the aorta and iliac arteries. Arterial wall compliance was calculated from pulse wave velocity in 45 apparently healthy men. Their arterial compliance fell significantly with advancing age, raised blood pressure, increased serum cholesterol and triglyceride levels, and reduced serum high density lipoprotein cholesterol levels. The correlation between compliance and age was independent of the other risk factors, and the correlation between compliance and Iipid status was independent of age and blood pressure. There was no significant correlation between compliance and area under the glucose tolerance curve. (Arteriosclerosis 6:105-108, January/February 1986)

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Section: Discussionmentioning

confidence: 99%

Risk factors for changes in aorto-iliac arterial compliance in healthy men.

Relf¹,

Lo²,

Myers³

et al. 1986

Arteriosclerosis

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“…Patients with coronary artery disease, when compared to controls in the same age group, also have been shown to have a higher pulse wave velocity, which was attributed to aortic atherosclerosis. 4 In contrast, other studies in man have shown that the presence of atherosclerosis does not result in abnormally high wave velocity 3 …”

mentioning

confidence: 92%

Aortic pulse wave velocity, elasticity, and composition in a nonhuman primate model of atherosclerosis.

Farrar¹,

Green²,

Bond³

et al. 1978

Circulation Research

119

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SUMMARY Aortic pulse wave velocity was determined in Macaca fascicularis monkeys fed either atherogenic or control diets for 36 months. The foot-to-foot velocity and apparent phase velocities of the second through seventh Fourier harmonics at a given diastolic pressure in the atherosclerotic monkeys were 1.5 to 2.0 times the values for the control animals. More than 80% of the aortic intimal surface of the atherosclerotic monkeys was covered with fibrous or fatty plaque, which approximately doubled wall thickness and wall thickness to radius ratio. Angiochemical evaluations showed no difference in collagen or elastin concentration (as a fraction of lipid and mineral-free dried aorta), but the atherosclerotic aortas were 1.5 to 2.0 times that of control in collagen and elastin content (defined as the absolute quantity beneath a square centimeter of intimal surface). Total cholesterol and calcium concentrations in the atherosclerotic aortas were more than 10 times the values for the control aortas. The static circumferential distensibility of the excised atherosclerotic aortas was significantly less than control, but there was no difference in incremental (Young's) modulus of elasticity. The in vitro pressure-strain elastic modulus of the atherosclerotic aortas was more than twice that of control, which was predicted from the enhanced wave velocity. The significantly increased stiffness of the atherosclerotic arteries appeared to be due mainly to the increased wall thickness caused by the atherosclerotic plaques rather than to material changes described by Young's modulus. Extensive medial damage, however, also was present and could have had a major influence on stiffness. Atherosclerosis therefore can result in increased aortic stiffening, detectable by pulse wave velocity, even if there is no change in the overall Young's modulus of elasticity.

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“…[1][2][3][4][5] Stiffness represents the fundamental mechanical property of the large arteries responsible for the non-resistive component of left ventricular load and of vascular performance during diastole. Stiffness is translated to its functional effect, or compliance, via geometric factors.…”

Section: Introductionmentioning

confidence: 99%