Carotid Intimal-Medial Thickness and Stiffness Are Not Affected by Hypercholesterolemia in Uncomplicated Essential Hypertension

Saba, Pier Sergio; Roman, Mary J.; Longhini, C; Scorzoni, Daniela; Pini, Riccardo; Devereux, Richard B.; Ganau, Antonello

doi:10.1161/01.atv.19.11.2788

Cited by 27 publications

(25 citation statements)

References 67 publications

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“…For example, the augmentation index and indices of arterial stiffness have been shown to be independent of cholesterol levels in patients with hypertension and/or hypercholesterolemia. 13,14 Furthermore, cholesterol lowering with statin did not change the augmentation index or central arterial compliance in patients with hypercholesterolemia. 15,16 In contrast, elevated LDL cholesterol has been associated with increased central PP, augmentation index, and PP amplification in various patient groups.…”

Section: Discussionmentioning

confidence: 95%

Impact of Statin Therapy on Central Aortic Pressures and Hemodynamics

et al. 2009

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Section: Discussionmentioning

confidence: 95%

Impact of Statin Therapy on Central Aortic Pressures and Hemodynamics

et al. 2009

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“…Another clinical study found that IMT in hypercholesterolemic hypertensives was not significantly thicker than IMT in normocholesterolemic hypertensives. 38 A synergism between SBP and LDL for atherosclerosis is not supported by findings from cohort studies with incident coronary disease or mortality as end points. For example, in the Honolulu Heart Program, serum cholesterol and SBP are additive (rather than synergistic) in logistic or probit models of coronary heart disease risk (J.H.…”

Section: Discussionmentioning

confidence: 99%

Blood Pressure, LDL Cholesterol, and Intima-Media Thickness

Park

Dwyer

Merz

et al. 2000

ATVB

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Abstract-The "response to injury" hypothesis is a plausible model of the development of atherosclerosis supported by observations from animal models. The present study uses epidemiological data to investigate the hypothesis that wall damage due to hypertension is a precursor of low density lipoprotein cholesterol (LDL-C)-mediated atherosclerosis. The Los Angeles Atherosclerosis Study is following a cohort of 576 participants who were aged 40 to 60 years and were free of symptomatic cardiovascular disease at recruitment. Key Words: atherosclerosis Ⅲ response-to-injury model Ⅲ intima-media thickness Ⅲ LDL cholesterol Ⅲ blood pressure A ccording to the "response-to-injury" model of atherogenesis, 1,2 various factors, which include hemodynamic forces and chemical agents, induce dysfunctional alterations in the overlying endothelium. This injury may then be followed by the aggregation of platelets, oxidized lipids, and smooth muscle cells in the intimal layer and by the eventual formation of plaques.This model of atherogenesis predicts that the atherosclerotic deposition of LDL cholesterol (LDL-C) may require previous damage to the endothelium by a factor such as hypertension. There are various experimental results from animal models of atherosclerosis that support the injury hypothesis. 3 For example, in the Watanabe heritable hyperlipidemic rabbit, plasma lipoproteins play a key role in determining the intimal response to hypertension. 4 Hypertension-induced changes in the intima lead to thickening but do not generally progress to atherosclerotic plaque formation in the absence of elevated plasma lipoproteins. 5 The roles of high blood pressure and LDL-C proposed in the response-to-injury hypothesis of atherosclerosis can be tested with B-mode ultrasound measurement of intima-media thickness (IMT) in the common carotid artery. 6 Increased IMT is characteristic of natural aging 7 and early atherosclerosis. 2 Such thickening of the common carotid arteries has been related prospectively to the risk of coronary heart disease events. 8 -10 In addition, carotid IMT has been related to cardiovascular risk factors in epidemiological studies, 11,12 and it has shown regression in lipid-lowering intervention trials. [13][14][15][16][17] Epidemiological data from cohorts with coronary disease morbidity or mortality events as end points may not detect an interaction between blood pressure and blood lipid levels because of the additional role of hypertension or hypercholesterolemia in the thromboembolic pathways that lead to events.Hypertension and elevated serum LDL-C are established as independent risk factors for thicker carotid artery intima-

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“…97 Accordingly, no significant correlation between cholesterol levels and local (carotid Young's elastic modulus and b stiffness index) 98 or systemic (total arterial compliance) 99 indices of arterial stiffness was found in populations with a high prevalence of atherosclerosis. Conversely, central pulse pressure and augmentation index have been found increased in patients with hypercholesterolemia.…”

Section: Impact Of Arterial Structure and Function On Ventricular Loamentioning

confidence: 99%

Ventricular–vascular coupling in hypertension

Saba

Cameli

Casalnuovo

et al. 2014

Journal of Cardiovascular Medicine

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The present review is addressed to analyse the complex interplay between left ventricle and arterial tree in hypertension. The different methodological approaches to the analysis of ventricular-vascular coupling in the time and frequency domain are discussed. Moreover, the role of hypertension-related changes of arterial structure and function (stiffness and wave reflection) on arterial load and how ventricular-vascular coupling modulates the process of left ventricular adaptation to hypertension are analysed.The different interplay between vascular bed and left ventricle emerges as the pathophysiological basis for the development of the multiple patterns of ventricular structural adaptation in hypertension and provides a pathway for the interpretation of systolic and diastolic functional abnormalities observed in hypertensive patients. Targeting the therapeutic approach to improve ventricularvascular coupling may have relevant impact on reversing left ventricular hypertrophy and improving systolic and diastolic dysfunction. J Cardiovasc Med 2014, 15:773-787

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Carotid Intimal-Medial Thickness and Stiffness Are Not Affected by Hypercholesterolemia in Uncomplicated Essential Hypertension

Cited by 27 publications

References 67 publications

Impact of Statin Therapy on Central Aortic Pressures and Hemodynamics

Impact of Statin Therapy on Central Aortic Pressures and Hemodynamics

Blood Pressure, LDL Cholesterol, and Intima-Media Thickness

Ventricular–vascular coupling in hypertension

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