The prevalence of concomitant hypertension and hypercholesterolaemia in the general population

Bacquer, Dirk De; Backer, Guy De

doi:10.1016/j.ijcard.2005.08.037

Cited by 20 publications

(17 citation statements)

References 15 publications

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“…In subjects with HT, it is generally recognized that firstly LV myocardial hypertrophy occurs, followed by diastolic dysfunction of the LV myocardium and finally systolic dysfunction of the LV myocardium [21][22][23][24][25][26][27][28]. The thickness of IVS, PW of LV and weight of the LV myocardium were significantly larger in subjects with primary HT in this study, in comparison with the control group, but the degree of thickness of IVS, PW of LV and weight of LV myocardium in the primary HT group did not fit the classical criteria of LV hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

Left atrial compensatory function in subjects with early stage primary hypertension assessed by using left atrial volumetric emptying fraction acquired by transthoracic echocardiography

Wakatsuki

Funabashi

Mikami

et al. 2009

International Journal of Cardiology

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Section: Discussionmentioning

confidence: 99%

Left atrial compensatory function in subjects with early stage primary hypertension assessed by using left atrial volumetric emptying fraction acquired by transthoracic echocardiography

Wakatsuki

Funabashi

Mikami

et al. 2009

International Journal of Cardiology

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“…In humans it is difficult to differentially study the effect of hypertension and hypercholesterolemia on the early phases of atherosclerosis development, because they are frequently associated in clinical practice, 13 cluster with other risk factors, and are recognized in later phases. 14 Therefore, we designed the present study to test the hypothesis that in the early phases of carotid atherosclerosis, hypertension, and hypercholesterolemia might differentially affect arterial function and structure.…”

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confidence: 99%

Hypertension and Hypercholesterolemia Differentially Affect the Function and Structure of Pig Carotid Artery

et al. 2007

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Abstract-The purpose of this work was to compare the effects of hypertension and hypercholesterolemia on carotid endothelial function, structure, and vasa vasorum density. Seventeen pigs were randomized to a 12-week normal diet without (nϭ5), or with renovascular hypertension (HT; nϭ6), or to a high cholesterol diet (HC; nϭ6). Carotid arteries were studied by organ chambers (endothelial function) and microcomputed tomography (vasa vasorum), and tissue was processed for Sirius red staining and immunoblotting (vascular endothelium growth factor, endostatin, matrix metalloproteinase-9, and matrix metalloproteinase-2). HC and HT showed reduced vasodilation to acetylcholine as compared with controls, but HT also had a lower response to sodium nitroprusside. In addition, HT showed a higher content of organized collagen fibers and increased intima-media thickness. Vasa vasorum density was increased in HC but not in HT. Both HT and HC showed a proangiogenetic biochemical milieu (higher vascular endothelium growth factor, matrix metalloproteinases, and lower endostatin), but this was more pronounced in HC. Both hypertension and hypercholesterolemia induce endothelial dysfunction in the carotid artery. However, hypertension is also associated with greater fibrosis and vascular wall thickening, which might impair endothelium-independent vasorelaxation and vasa vasorum growth. Hypercholesterolemia is, in turn, associated with vasa vasorum neovascularization. These data suggest that carotid atherosclerosis can evolve through different mechanisms in relation to different risk factors. Key Words: carotid artery Ⅲ atherosclerosis Ⅲ hypertension Ⅲ hypercholesterolemia Ⅲ vasa vasorum Ⅲ endothelium S troke is a leading cause of death in Western countries, and in the majority of the cases it is the consequence of an acute complication of an atherosclerotic carotid plaque. Risk factors for carotid atherosclerosis include the traditional cardiovascular risk factors, and, in particular, hypertension plays a major role. 1 Although in the past hypercholesterolemia was not considered a determinant contributor to cerebrovascular disease, 2,3 recent epidemiological studies and clinical trials with lipid-lowering drugs demonstrated a clear relation between serum cholesterol levels and carotid atherosclerosis, as well as with the risk of stroke. 1 Both hypertension and hypercholesterolemia are characterized by similar proatherogenic hallmarks, including endothelial dysfunction, vascular inflammation, and oxidative stress. However, the consequences of the action of these 2 risk factors on the arterial wall might be substantially different. Indeed, different cardiovascular risk factors influence atherosclerosis development favoring preferential plaque characteristics, eventually leading to the formation of morphologically different lesions. 4,5 Experimental analysis of the interaction between hypertension and hypercholesterolemia on the mechanisms of early atherosclerosis indicates that hypertension, per se, induces adaptive remodeling, whe...

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“…While much has been learned about the influence of each risk factor on vascular function, less attention has been devoted to addressing the combined actions of HTN and HCh on the vasculature. Such an effort is justified based on epidemiological studies that reveal a high prevalence of co-existing HTN and HCh in the human population, with approximately 30–40% of men and women showing both risk factors(10). Clinical evidence also indicates that the concurrence of HTN and HCh increases the incidence of atherosclerosis and cardiac events, relative to the changes noted with either risk factor alone(27).…”

Section: Discussionmentioning

confidence: 99%

Hypercholesterolemia blunts the oxidative stress elicited by hypertension in venules through angiotensin II type-2 receptors

Yıldırım

Senchenkova

Granger

2016

Microvascular Research

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OBJECTIVE Hypertension and hypercholesterolemia elicit inflammatory and thrombogenic responses in the microvasculature. However, little is known about whether and how risk factor combinations alter microvascular function. We examined how the actions of HTN+HCh on the microvasculature differ from the responses elicited by either risk factor alone. METHODS Intravital microscopy was used to monitor the adhesion and emigration of leukocytes and dihydrorhodamine oxidation in cremaster muscle venules of wild type mice that were infused with angiotensin II for 2 wks (HTN), placed on a high cholesterol diet (HCD), or both. RESULTS Either HTN or HCh alone enhanced the production of reactive oxygen species and promoted the recruitment of leukocytes in venules. However, the combination of HTN and HCh produced changes in ROS production and leukocyte recruitment that were greatly attenuated compared to HTN alone. The inhibitory effects of HCh on the AngII mediated responses were also observed in genetically-induced HCh (ApoE-deficient mice). Treating HCh + HTN mice with an antagonist to AT2r reversed the HCh-dependent protection against oxidative stress and inflammation during HTN. CONCLUSIONS These findings indicate that HCh blunts the oxidative stress and inflammatory cell recruitment elicited by hypertension in venules through a mechanism that involves AT2 receptor activation.

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The prevalence of concomitant hypertension and hypercholesterolaemia in the general population

Cited by 20 publications

References 15 publications

Left atrial compensatory function in subjects with early stage primary hypertension assessed by using left atrial volumetric emptying fraction acquired by transthoracic echocardiography

Left atrial compensatory function in subjects with early stage primary hypertension assessed by using left atrial volumetric emptying fraction acquired by transthoracic echocardiography

Hypertension and Hypercholesterolemia Differentially Affect the Function and Structure of Pig Carotid Artery

Hypercholesterolemia blunts the oxidative stress elicited by hypertension in venules through angiotensin II type-2 receptors

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