Inverse relationship between ambulatory arterial stiffness index and glomerular filtration rate in arterial hypertension.

BACKGROUND: Arterial stiffness and mild-to-moderate renal dysfunction are predictors of cardiovascular (CV) morbidity and mortality. Recently, the ambulatory arterial stiffness index (AASI) has been proposed as a surrogate index of arterial stiffness. It has been associated with an enhanced risk of stroke. The aim of our study was to assess the relationship between AASI and glomerular filtration rate (GFR) in a group of hypertensive patients with no CV complications. METHODS: A total of 143 untreated hypertensive subjects (mean age: 44 +/- 12 years; men 57%), with serum creatinine <1.5 mg/dl, were enrolled. AASI was calculated as one minus the regression slope of diastolic on systolic blood pressure (BP) obtained by individual 24-h BP recordings. GFR was computed from the scintigraphic determination of the technetium-99m diethylenetriaminepentaacetic acid uptake within the kidneys, by the Gates' method. RESULTS: Hypertensive patients with AASI above the median value (n = 71) had lower GFR than those with AASI below the median (n = 72) (98.3 +/- 31 vs. 122.4 +/- 32 ml/min/1.73 m(2); P < 0.001). This difference held even after adjustment for age and gender. The linear regression analysis disclosed a significant inverse correlation between GFR and AASI (r = -0.30; P < 0.001), that was replicated (beta = -0.19; P = 0.02) in a multiple regression model including, as independent variables (besides AASI), age, gender, high-density lipoprotein cholesterol, body mass index, 24-h pulse pressure (PP) and nocturnal reduction in BP. CONCLUSIONS: AASI is inversely related to GFR in arterial hypertension. This may help to explain the increased CV risk associated with mild-to-moderate renal dysfunction.

Impact of the metabolic syndrome on total arterial compliance in essential hypertension patients.

The aim of the study was to cross-sectionally analyze, in a group of essential hypertension patients without diabetes mellitus, the influence of the metabolic syndrome (MS) on the stroke volume index to pulse pressure (SVi/PP) ratio, a measure of total arterial compliance. A total of 528 essential hypertension patients, aged 18 to 72 years, free from cardiovascular and renal disease (41% of whom had MS) were enrolled. All participants underwent routine blood chemistry, echocardiographic examination, and 3 blood pressure measurements at the end of echocardiographic examination. When compared with participants who did not have MS, hypertensive patients with MS exhibited lower SVi/PP ratio (0.65+/-0.22 vs 0.73+/-0.21 mm Hg; P=.0003). The independent association of MS with SVi/PP ratio (beta=0.10; P=.02) was confirmed in a multivariate regression model including age, sex, and other potential confounders as covariates. The authors' finding may help to explain the enhanced cardiovascular risk associated with MS.

Relationship of metabolic syndrome with pulse pressure in patients with essential hypertension.

BACKGROUND: Pulse pressure is largely dependent on arterial stiffness. Recent studies have documented reduced large artery compliance in nondiabetic subjects with metabolic syndrome (MS). The aim of our study was to analyze, in a group of patients with essential hypertension and without diabetes mellitus, the influence of MS on clinic and 24-h pulse pressures. METHODS: A total of 528 hypertensive subjects, aged 18 to 72 years, who were free of cardiovascular and renal diseases were enrolled. Of the subjects, 41% had MS. In all subjects routine blood chemistry, echocardiographic examination, and 24-h ambulatory blood pressure monitoring were performed. RESULTS: When compared with subjects without MS, hypertensive patients with MS exhibited more elevated clinic pulse pressures (66 +/- 16 v .58 +/- 14 mm Hg; P < .00001) and 24-h (51 +/- 9 v .48 +/- 7 mm Hg; P = .00001). These results held even after correction for age, sex, stroke volume, mean pressures, and total cholesterol. The regression line relating PP with age was steeper in patients with MS than in those without MS. Multivariate regression models confirmed that the relationships of MS with clinic (beta = 0.12; P = .003) and 24-h PP (beta = 0.11; P = .01) were independent from several confounding factors. CONCLUSIONS: The elevated levels of clinic and 24-h PP observed in hypertensive patients with MS may reflect increased large arteries stiffness and may therefore contribute to explain the enhanced cardiovascular risk associated with MS.

Impact of metabolic syndrome on left ventricular mass in overweight and obese hypertensive subjects.

BACKGROUND: Metabolic syndrome (MS) has been associated with an increased left ventricular (LV) mass in recent reports. Little is known about the association of MS with LV mass (LVM) in overweight and obese individuals. The aim of our study was to investigate the relation between MS and LVM in a population of overweight and obese hypertensive subjects. METHODS: 289 non-diabetic essential hypertensives with a body mass index >25 kg/m2, were enrolled. In all subjects routine blood chemistry, echocardiographic examination and 24-h ambulatory blood pressure monitoring were performed. RESULTS: In the group of overweight patients, participants with MS (n=58), when compared to those without it (n=127), exhibited significantly greater LVM indexed for height(2.7) (LVMH(2.7)) (50+/-12 vs 44+/-11 g/m(2.7); p=0.0001), even after controlling for age, gender and 24-h systolic blood pressure. Similar results were obtained in the group of obese individuals, being LVMH(2.7) (56+/-12 vs 44+/-9 g/m(2.7); p<0.0001) greater in subjects with MS (n=77) than in those without MS (n=27), even after adjustment for age, gender and clinic systolic blood pressure. The independent association of MS with LVMH(2.7) in overall study population was confirmed by linear multiple regression analyses (beta=0.20; p=0.0004). CONCLUSIONS: MS seems to increase LVM over and above the potential contribution of blood pressure, body size and other single components of this syndrome. Since LV hypertrophy is a well-known predictor of cardiovascular events, our results may partly explain the enhanced cardiovascular risk associated with MS.