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      Microalbuminuria Is Closely Related to Impaired Arterial Elasticity in Untreated Patients with Essential Hypertension

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          Abstract

          Background/Aim: Although an increase in urinary albumin excretion (UAE) and impaired arterial mechanics have both been identified as predictors of cardiovascular events in hypertensive subjects, the interaction between arterial pressure wave contour and microalbuminuria (MA) has not been well defined. Methods: MA was determined from three nonconsecutive 24-hour urine samples in a group of 130 untreated hypertensive subjects. The arterial pressure waveform was recorded by carotid artery applanation tonometry and expressed as the augmentation index (AIx), the ratio of the augmented pressure (the difference between the early and late systolic shoulder) to pulse pressure. The subjects were classified according to their arterial pressure waveform into type A (Aix >0.12), type B (0 < Aix ≤ 0.12), and type C (Aix ≤ 0). Results: Patients with MA (n = 48) were matched for demographics with those without MA (n = 82). Subjects with MA had significantly increased left ventricular mass index (101 vs. 85 g/m<sup>2</sup>, p < 0.0001), blood pressure (164/100 vs. 146/94 mm Hg, p < 0.005), and AIx (0.16 vs. 0.04, p < 0.03). Hypertensive patients with type A arterial pressure waveform had significantly increased values of the log 24-hour UAE as compared with those with type B and C pressure waveforms. The proportion of patients with type A waveform was significantly higher in microalbuminuric patients as compared with normoalbuminuric patients (67 vs. 33%, p < 0.005); in contrast, the proportion of patients with type B or C waveform was significantly higher in normoalbuminuric patients as compared with microalbuminuric patients (68 vs. 36%, p < 0.005). By multiple regression analysis and analysis of variance, it was revealed that an increased AIx was significantly and independently associated with increased values of UAE (p < 0.05). Conclusions: Hypertensive patients with MA exhibited an earlier systolic augmentation of the arterial pressure, reflecting a more impaired arterial elasticity as compared with hypertensive subjects without MA. These findings suggest that worse cardiovascular outcomes may be associated with the presence of an increased UAE in hypertensive subjects.

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          Most cited references 4

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          Microalbuminuria and endothelial dysfunction in essential hypertension.

          Microalbuminuria (urinary albumin excretion between 20 and 200 micrograms/min) and endothelial dysfunction coexist in patients with essential hypertension. To evaluate whether the two phenomena are related and the determinants of that association, we recruited 10 untreated males with essential hypertension and microalbuminuria without diabetes to be compared with an equal number of matched patients with essential hypertension excreting albumin in normal amounts and 10 normal controls. The status of endothelial function was inferred from circulating von Willebrand Factor antigen (vWF), a glycoprotein secreted in greater amounts when the vascular endothelium is damaged. vWF concentrations were higher in hypertensive patients with microalbuminuria than in hypertensive patients without and controls. Individual vWF and urine albumin-excretion values were correlated (r = 0.55, p < 0.002). Blood pressure correlated with both urinary albumin excretion and vWF. Left ventricular mass index and minimal forearm vascular resistances were comparable in patients with hypertension and higher than in controls; total and low-density lipoprotein cholesterol, triglycerides, lipoprotein-a, Factor VII, and plasminogen activator inhibitor-1 did not differ. Fibrinogen was higher and creatinine clearance lower in microalbuminurics. Albuminuria in essential hypertension may reflect systemic dysfunction of the vascular endothelium, a structure intimately involved in permeability, haemostasis, fibrinolysis, and blood pressure control. This abnormality may have important physiopathological implications and expose these patients to increased cardiovascular risk.
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            Influence of age and end-stage renal disease on the stiffness of carotid wall material in hypertension.

            Incremental elastic modulus, which is the slope of the relationship between stress and strain of arterial vessels, is a marker of wall material stiffness. The radial artery incremental elastic modulus, which is not influenced by age, is normal or reduced in patients with essential hypertension but increased in patients with end-stage renal disease. Authors of studies on hypertension largely ignore the question of whether the incremental elastic modulus, measured in the common carotid artery as typical of a central artery site, differs according to age or to the presence of end-stage renal disease or both. The carotid incremental elastic modulus was measured in 208 hypertensive patients divided into four groups according to age ( 55 years) and the presence or absence of end-stage renal disease. The incremental elastic modulus was calculated from transcutaneous measurements of arterial internal diameter and wall thickness (echo-tracking device) and carotid pulse pressure (tonometry). Because the four groups of subjects had the same mean arterial pressure, the static incremental elastic modulus was calculated both in isobaric conditions and for the same wall stress. In nonuremic subjects, lumen diameter, wall thickness and the incremental elastic modulus were significantly (P < 0.001) increased in older subjects whereas compliance and distensibility were decreased. The mean (+/- SD) elastic modulus was 0.41 +/- 0.14 x 10(3) kPa in younger and 0.71 +/- 0.28 x 10(3) kPa in older subjects. In uremic subjects, the corresponding values were 0.48 +/- 0.30 and 0.90 +/- 0.49 x 10(3) kPa, and therefore higher than in nonuremic subjects, irrespective of age. Multiple regression analysis showed that age, mean arterial pressure and the presence of end-stage renal disease independently influenced carotid diameter, distensibility and the incremental elastic modulus. In hypertensive patients, the carotid incremental elastic modulus is increased independently in aging men and women and in the presence of uremia. This increase is not dependent on mechanical factors such as the level of mean blood pressure.
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              Arterial mechanics predict cardiovascular risk in hypertension

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                Author and article information

                Journal
                NEC
                Nephron Clin Pract
                10.1159/issn.1660-2110
                Nephron Clinical Practice
                S. Karger AG
                1660-2110
                2003
                March 2003
                17 November 2004
                : 93
                : 3
                : c106-c111
                Affiliations
                Department of Cardiology, Hippokration Hospital, University of Athens, Athens, Greece
                Article
                69546 Nephron Clin Pract 2003;93:c106–c111
                10.1159/000069546
                12660419
                © 2003 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 3, References: 28, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/69546
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