Influence of the metabolic syndrome on aortic stiffness in never treated hypertensive patients

Mulè, Giuseppe; Cottone, Santina; Mongiovì, Rosalia; Cusimano, Paola; Mezzatesta, Giovanni; Seddio, Giovanna; Volpe, Vito; Nardi, Emilio; Andronico, Giuseppe; Piazza, G.; Cerasola, Giovanni

doi:10.1016/j.numecd.2005.03.005

Cited by 52 publications

(43 citation statements)

References 22 publications

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“…muscular and elastic arteries within the same group of individuals in contrast to most, 5,6,[9][10][11][12][14][15][16] but not all, 7,8,13 earlier studies, which examined arterial stiffness at only one arterial site [14][15][16] or at one arterial segment. 5,6,[9][10][11][12]16 Our data suggest that increased arterial stiffness may link the MetS to CVD and is in general agreement with the above studies. In addition, our data supports the observation that muscular arteries-in particular the femoral artery-seem to stiffen preferentially over elastic arteries.…”

Section: Discussionmentioning

confidence: 91%

“…3 The term arterial stiffness refers to an impairment in the cushioning function of the artery (that is, a diminished ability to convert the pulsatile blood flow from the heart into a steady and continuous stream throughout the arterial tree), which leads to increased systolic blood pressure, left ventricular hypertrophy, impaired coronary perfusion and arterial stiffness-associated CVD (notably, stroke, heart failure and myocardial infarction), 4 and can be measured both locally (at a single location within the artery wall) or regionally (over a prespecified arterial segment, for example, the carotid-femoral tract). Earlier studies on arterial stiffness in the MetS [5][6][7][8][9][10][11][12][13][14][15][16] have raised several issues. Firstly, there is some evidence that, in the MetS, increases in arterial stiffness may not be uniformly distributed over muscular (that is, peripheral) and elastic (that is, central) arteries.…”

Section: Introductionmentioning

confidence: 99%

“…Firstly, there is some evidence that, in the MetS, increases in arterial stiffness may not be uniformly distributed over muscular (that is, peripheral) and elastic (that is, central) arteries. 7,8,13 The interpretation of the literature, however, is hampered by the fact that most studies reported arterial stiffness in only one site [14][15][16] or segment, 5,6,[9][10][11][12] whereas studies that did report on multiple sites 8 or segments 7,13 showed discordant results. Secondly, the MetS is associated with insulin resistance (IR), a proinflammatory state and endothelial dysfunction (ED), 17 and it has been suggested that these phenomena play an important role in the complex pathobiology of arterial stiffening.…”

Section: Introductionmentioning

confidence: 99%

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The metabolic syndrome in elderly individuals is associated with greater muscular, but not elastic arterial stiffness, independent of low-grade inflammation, endothelial dysfunction or insulin resistance—The Hoorn Study

et al. 2009

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The metabolic syndrome (MetS) increases cardiovascular disease (CVD) risk. How MetS increases CVD risk is incompletely understood, but increasing arterial stiffness is one candidate link, which in turn could be explained by (low-grade) inflammation, endothelial dysfunction (ED) or insulin resistance (IR). However, MetSrelated increases in stiffness may not be uniformly distributed over muscular and elastic arteries. Therefore, the purpose of this study was to determine: (1) the associations between the MetS, and muscular and elastic arterial stiffness, and (2) whether any such associations could be explained by inflammation, ED or IR. These questions were addressed in the Hoorn Study. MetS was defined according to the NCEP (National Cholesterol Education Program) criteria. Arterial stiffness was determined by ultrasound, tonometry and echocardiography. Inflammation, ED and IR were estimated by C-reactive protein, flow-mediated vasodilation and the homoeostatic model for the assessment of IR, respectively. The results showed that MetS was associated with both femoral and brachial arterial stiffness, significantly so for the distensibility coefficients and for the femoral compliance coefficient. In the carotid artery and aorta, no particular pattern emerged. Additional adjustment for either inflammation, ED or IR did not materially alter the results. The results therefore indicate that muscular arteries may stiffen preferentially over elastic arteries and that distensibility is affected to a greater extent than compliance, thus maintaining volume compliance over vessel wall stiffening. Additionally, the increase in stiffness was not explained by inflammation, ED or IR and suggests that stiffening of the muscular arteries in MetS may not be the consequence of these phenomena.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The metabolic syndrome in elderly individuals is associated with greater muscular, but not elastic arterial stiffness, independent of low-grade inflammation, endothelial dysfunction or insulin resistance—The Hoorn Study

et al. 2009

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“…[3][4][5][6][7] Despite recent evidence of a major impact on cardiovascular risk, [8][9][10] there is debate in the scientific community about whether identification of the metabolic syndrome improves prediction of cardiovascular events compared to use of single risk factors. [11][12][13][14] Paralleling this debate, however, there is emerging evidence that the metabolic syndrome is associated with preclinical cardiovascular disease [15][16][17][18][19][20] and higher rates of cardiovascular events, [8][9][10] suggesting that the metabolic syndrome may have more adverse cardiovascular effects than predicted by its individual components.…”

Section: Introductionmentioning

confidence: 99%

Clusters of metabolic risk factors predict cardiovascular events in hypertension with target-organ damage: the LIFE study

et al. 2007

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The relation of metabolic syndrome (MetS) with cardiovascular outcome may be less evident when preclinical cardiovascular disease is present. We explored, in a post hoc analysis, whether MetS predicts cardiovascular events in hypertensive patients with electrocardiographic left ventricular hypertrophy (ECG-LVH) in the Losartan Intervention For Endpoint (LIFE) reduction in hypertension study. MetS was defined by X2 risk factors plus hypertension: body mass index X30 kg/m 2 , high-density lipoprotein (HDL)-cholesterol o1.0/1.3 mmol/l (o40/ 50 mg/dl) (men/women), glucose X6.1 mmol/l (X110 mg/ dl) fasting or X7.8 mmol/l (X140 mg/dl) nonfasting or diabetes. Cardiovascular death and the primary composite end point (CEP) of cardiovascular death, stroke and myocardial infarction were examined. In MetS (1591 (19.3%) of 8243 eligible patients), low HDL-cholesterol (72%), obesity (77%) and impaired glucose (73%) were similarly prevalent, with higher blood pressure, serum creatinine and Cornell product, but lower Sokolow-Lyon voltage (all Po0.001). After adjusting for baseline covariates, hazard ratios for CEPs and cardiovascular death (4.871.1 years follow-up) were 1.47 (95% confidence interval (CI), 1.27-1.71)-and 1.73 (95% CI, 1.38-2.17)-fold higher with MetS (both Po0.0001), and were only marginally reduced when further adjusted for diabetes, obesity, low HDL-cholesterol, non-HDL-cholesterol, pulse pressure and in-treatment systolic blood pressure and heart rate. Thus, MetS is associated with increased cardiovascular events in hypertensive patients with ECG-LVH, independently of single cardiovascular risk factors.

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“…Increased arterial stiffness, previously reported in hypertensive subject with MetS, 12,31,32 or non-haemodynamic factors, 14 may be responsible for the increased LVM observed in individuals with MetS. It is well known that insulin resistance and the accompanying compensatory hyperinsulinemia are the pathophysiological key features underlying MetS.…”

Section: Discussionmentioning

confidence: 89%

Relationships between metabolic syndrome and left ventricular mass in hypertensive patients: does sex matter?

et al. 2008

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Several studies documented an association between metabolic syndrome (MetS) and left ventricular (LV) hypertrophy. However, only in a few of these studies the impact of MetS on left ventricular mass (LVM) was separately analysed by gender, with conflicting results. The aim of our study was to verify, in a wide sample of essential hypertensive patients, the influence of gender, if any, on the relationship between MetS and LVM. We enrolled 475 non-diabetic subjects (mean age: 46 ± 11 years), with mild-to-moderate essential hypertension, of whom 40% had MetS, defined on the basis of Adult Treatment Panel III (ATPIII) criteria. All the patients underwent a 24-h ambulatory blood pressure monitoring and an echocardiogram. LVM indexed for height 2.7 (LVMH 2.7 ) was significantly (Po0.001) higher in women with MetS (n ¼ 83) than in those without it (n ¼ 97; 54 ± 17 vs 42±11 g m À2.7). An equally significant difference in LVMH 2.7 was documented also in male gender between the two groups with (n ¼ 105) and without MetS (n ¼ 190; 51 ± 14 vs 43±11 g m À2.7 ; Po0.001). The relationship between MetS and LVMH 2.7 remained statistically significant (Po0.001) in both sexes, in multiple regression analyses, even after adjustment for potential confounding factors. Our results seem to suggest that the relationship between MetS and LVM is not significantly affected by gender, being LVM increased in both hypertensive women and men with MetS.

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Influence of the metabolic syndrome on aortic stiffness in never treated hypertensive patients

Cited by 52 publications

References 22 publications

The metabolic syndrome in elderly individuals is associated with greater muscular, but not elastic arterial stiffness, independent of low-grade inflammation, endothelial dysfunction or insulin resistance—The Hoorn Study

The metabolic syndrome in elderly individuals is associated with greater muscular, but not elastic arterial stiffness, independent of low-grade inflammation, endothelial dysfunction or insulin resistance—The Hoorn Study

Clusters of metabolic risk factors predict cardiovascular events in hypertension with target-organ damage: the LIFE study

Relationships between metabolic syndrome and left ventricular mass in hypertensive patients: does sex matter?

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