Endothelial Control of Arterial Distensibility Is Impaired in Chronic Heart Failure

Ramsey, Mike; Goodfellow, Jonathan; Jones, Christopher J.; Luddington, Lisa; Mj, Lewis; Henderson, A. H.

doi:10.1161/01.cir.92.11.3212

Cited by 238 publications

(185 citation statements)

References 25 publications

Supporting

Mentioning

169

Contrasting

Unclassified

Order By: Relevance

“…endothelial dysfunction, or by promoting smooth muscle cell proliferation. 23,[25][26][27][28] A recent study by Ramsey et al 29 showed that arterial distensibility is controlled by normal endothelium in healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

Large-Artery Elastic Properties in Young Men

Toikka

Niemi

Ahotupa

et al. 1999

ATVB

View full text Add to dashboard Cite

Abstract-Measures of arterial elasticity have been proposed as surrogate markers for asymptomatic atherosclerosis. We investigated the relations of serum lipoproteins, oxidized low-density lipoprotein (ox-LDL), and familial hypercholesterolemia (FH) to arterial elasticity among young men. As a marker of arterial elasticity we measured compliance in the thoracic aorta by using magnetic resonance imaging and in the common carotid artery by using ultrasound. LDL diene conjugation was used as a marker of ox-LDL. In study I, 25 healthy men (aged 29 to 39) were classified into 2 extreme groups according to previously measured high-density lipoprotein cholesterol to total cholesterol ratio (HDL-C/TC ratio). In study II, the healthy men were used as controls for 10 age matched asymptomatic patients with FH. In healthy men, the group with low HDL-C/TC ratio had decreased carotid artery compliance (2.3Ϯ0.4% versus 1.9Ϯ0.5%/ 10 mm Hg, Pϭ0.034). In univariate analysis, the compliance of the carotid artery associated with ox-LDL (r ϭϪ0.49, Pϭ0.016) and HDL-C/TC ratio (rϭ0.41, Pϭ0.040). In multivariate regression analyses, ox-LDL was the only independent determinant for compliance of the carotid artery (Pϭ0.016). Aortic elasticity was not related to standard lipid variables, but the compliance of the ascending aorta associated with ox-LDL (rϭϪ0.44, Pϭ0.030). In FH patients, arterial elasticity was similar to that in controls. We conclude that elasticity of the common carotid artery is affected by serum lipid profile in young men. The current study demonstrates for the first time an in vivo association between ox-LDL and arterial elasticity suggesting that oxidative modification of LDL may play a role in the alteration of arterial wall elastic properties.

show abstract

Section: Discussionmentioning

confidence: 99%

Large-Artery Elastic Properties in Young Men

Toikka

Niemi

Ahotupa

et al. 1999

ATVB

View full text Add to dashboard Cite

show abstract

“…19 A number of other studies have described a relationship between various indices of arterial stiffness and endothelial dysfunction in selected patient groups. [21][22][23][24][25] However, these studies require invasive procedures and/or highly specialized equipment and operators. Moreover, only a limited number of studies assessed aortic PWV, the current gold-standard measure of large artery stiffness, and wave reflection characteristics.…”

Section: Mceniery Et Al Endothelial Function and Arterial Stiffnessmentioning

confidence: 99%

“…However, direct evidence of a relationship between endothelial function and more definitive measures of arterial stiffness is largely limited to studies in patients with cardiovascular disease and risk factors, [21][22][23][24][25][26] and the relationship between endothelial function and aortic (carotid-femoral) pulse wave velocity (PWV), the current "gold-standard" measure of stiffness, in healthy normotensive individuals, who are free of the potentially confounding influence of cardiovascular disease, has not been well-described. Moreover, as we 27 and others 28 have shown previously, brachial pulse pressure does not always provide an accurate indication of central pulse pressure, and the relationship between endothelial function and central pulse pressure is unclear.…”

mentioning

confidence: 99%

Endothelial Function Is Associated With Pulse Pressure, Pulse Wave Velocity, and Augmentation Index in Healthy Humans

et al. 2006

View full text Add to dashboard Cite

Abstract-Arterial stiffness is an independent predictor of mortality and is regulated by a number of factors, including vascular smooth muscle tone. However, the relationship between endothelial function and definitive measures of arterial stiffness and wave reflections has not been described in healthy individuals. Therefore, we tested the hypothesis that endothelial function is inversely correlated with aortic pulse wave velocity (PWV), central pulse pressure, and augmentation index in healthy individuals. Peripheral and central pulse pressure and augmentation index were determined at rest, and global endothelial function was measured using pulse wave analysis and administration of sublingual nitroglycerin and inhaled albuterol. Aortic PWV was also determined at baseline in a subset of 89 subjects.In a separate group of subjects (nϭ89), aortic PWV was measured and brachial artery flow-mediated dilatation assessed as a measure of conduit artery endothelial function. Key Words: nitric oxide Ⅲ endothelium-derived factors Ⅲ blood pressure Ⅲ pulse Ⅲ arteries E ndothelial dysfunction, characterized by a reduced bioavailability of endothelium-derived NO, is an important step in the progression of atherosclerosis. Indeed, resistance vessel, 1 conduit artery, 2 and coronary 3,4 endothelial dysfunction independently predict all-cause and cardiovascular mortality. A number of risk factors for cardiovascular disease, including age, 5 hypertension, 1 obesity, 6 hypercholesterolemia, 7 diabetes, 8 and smoking, 9 are associated with systemic endothelial dysfunction. Interestingly, these risk factors are also associated with increased elastic artery stiffness, 10,11 which is itself an important predictor of outcome in a number of patient groups. [12][13][14][15] Removal of the vascular endothelium alters arterial stiffness in animal models, 16 and we have demonstrated recently that blocking NO synthesis increases local arterial stiffness, 17,18 suggesting that endotheliumderived NO contributes to the regulation of large artery stiffness in vivo.Support for this hypothesis stems from the observation that brachial artery pulse pressure, a surrogate measure of large artery stiffness, correlates with coronary 19 and resistance vessel 20 endothelial function in hypertensive patients and controls. However, direct evidence of a relationship between endothelial function and more definitive measures of arterial stiffness is largely limited to studies in patients with cardiovascular disease and risk factors, [21][22][23][24][25][26] and the relationship between endothelial function and aortic (carotid-femoral) pulse wave velocity (PWV), the current "gold-standard" measure of stiffness, in healthy normotensive individuals, who are free of the potentially confounding influence of cardiovascular disease, has not been well-described. Moreover, as we 27 and others 28 have shown previously, brachial pulse pressure does not always provide an accurate indication of central pulse pressure, and the relationship between endothelial function and c...

show abstract

“…The validity of this method has been confirmed in previous studies. 20,21 Briefly, the diameter of the brachial artery was measured from B-mode ultrasound images with a 7.5-MHz linear array transducer (SSH-160A, Toshiba). Flow velocity in the brachial artery was measured with a pulsed Doppler signal at a 70°angle to the vessel, with the range gate (1.5 mm) in the center of the artery.…”

Section: Endothelial Functionmentioning

confidence: 99%

Evidence for an Independent and Cumulative Effect of Postprandial Hypertriglyceridemia and Hyperglycemia on Endothelial Dysfunction and Oxidative Stress Generation

et al. 2002

View full text Add to dashboard Cite

Background-Postprandial hypertriglyceridemia and hyperglycemia are considered risk factors for cardiovascular disease.Evidence suggests that postprandial hypertriglyceridemia and hyperglycemia induce endothelial dysfunction through oxidative stress; however, the distinct role of these two factors is a matter of debate. Methods and Results-Thirty type 2 diabetic patients and 20 normal subjects ate 3 different meals: a high-fat meal; 75 g glucose alone; and high-fat meal plus glucose. Glycemia, triglyceridemia, nitrotyrosine, and endothelial function were assayed during the tests. Subsequently, diabetics took 40 mg/d simvastatin or placebo for 12 weeks. The 3 tests were performed again at baseline, between 3 to 6 days after the start, and at the end of each study. High-fat load and glucose alone produced a decrease of endothelial function and an increase of nitrotyrosine in normal and diabetic subjects. These effects were more pronounced when high fat and glucose were combined. Short-term simvastatin treatment had no effect on lipid parameters but reduced the effect on endothelial function and nitrotyrosine observed during each different test. Long-term simvastatin treatment was accompanied by a lower increase in postprandial triglycerides, which was followed by smaller variations of endothelial function and nitrotyrosine during the tests. Conclusions-This study shows an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial function, suggesting oxidative stress as common mediator of such effect. Simvastatin shows a beneficial effect on oxidative stress and endothelial dysfunction, which may be ascribed to a direct effect as well as the lipid-lowering action of the drug.

show abstract

Endothelial Control of Arterial Distensibility Is Impaired in Chronic Heart Failure

Cited by 238 publications

References 25 publications

Large-Artery Elastic Properties in Young Men

Large-Artery Elastic Properties in Young Men

Endothelial Function Is Associated With Pulse Pressure, Pulse Wave Velocity, and Augmentation Index in Healthy Humans

Evidence for an Independent and Cumulative Effect of Postprandial Hypertriglyceridemia and Hyperglycemia on Endothelial Dysfunction and Oxidative Stress Generation

Contact Info

Product

Resources

About