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      Effects of Losartan Titrated to Losartan/Hydrochlorothiazide and Amlodipine on Left Ventricular Mass in Patients with Mild-to-Moderate Hypertension

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          Abstract

          To study the effects of the angiotensin II receptor antagonist Losartan and Amlodipine on left ventricular mass (LVM), we performed blood pressure measurements and transthoracic echocardiographies at baseline. After a 4-week placebo run-in period, 25 patients with mild-to-moderate essential hypertension were randomly allocated to active treatment with Losartan 50 mg titrated to Losartan 50 mg/hydrochlorothiazide (HCT) 12.5 mg (n = 11) or Amlodipine 5 mg titrated to 10 mg (n = 14) for 16 weeks. After treatment, blood pressure decreased significantly in both groups. LVM and LVM index (mean ± SD/median) in the Losartan group at baseline were 311 ± 101/288 g and 163 ± 55/150 g/m<sup>2</sup> and decreased significantly to 252 ± 25/255 g and 133 ± 22/128 g/m<sup>2</sup> (p = 0.003 for LVM; p = 0.01 for LVM index) after 16 weeks of active treatment. In the Amlodipine group LVM and LVM index decreased from 259 ± 47/243 g and 136 ± 25/ 131 g/m<sup>2</sup> to 240 ± 42/234 g and 126 ± 24/123 g/m<sup>2</sup> (n.s.). In conclusion, LVM decreased significantly as early as 16 weeks after initiation of antihypertensive treatment with the Angiotensin II antagonist Losartan.

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          Most cited references 5

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          White-coat hypertension as a cause of cardiovascular dysfunction.

           B Reid,  J Curzio,  S Glen (1996)
          The increasing use of 24 h ambulatory blood pressure monitoring has allowed diagnosis of white-coat hypertension, in which blood pressures are higher on clinic measurements than on ambulatory monitoring. Treatment is not generally thought to be necessary for this disorder. However, there is evidence that patients with white-coat hypertension develop renal impairment and left ventricular hypertrophy. We undertook this study to assess whether white-coat hypertension, in the absence of cardiovascular structural abnormalities, is associated with cardiovascular functional abnormalities. Cardiovascular function was assessed by ultrasonography in three groups of patients classified as normotensive, persistently hypertensive, or white-coat hypertensive (23, 20, and 22 patients, respectively) on the basis of ambulatory blood pressure monitoring, carried out for 28 h with recordings taken every 15 min during the day and every 20 min during the night, and clinic measurements, made with a semi-automatic oscillometric device. Similar abnormalities of diastolic left ventricular function were identified in the patients with persistent hypertension and those with white-coat hypertension; both groups differed in these indices from the normotensive group (E/A ratios 0.94 [SD 0.23], 1.06 [0.21], and 1.24 [0.31] respectively; ANOVA p < 0.005). In addition, the white-coat and persistently hypertensive groups, when compared with the normotensive group, showed similar abnormalities of elasticity, compliance, and stiffness (stiffness index 4.32 [1.90], 4.53 [1.38], and 3.27 [0.95] respectively; ANOVA p < 0.05) of the large arteries. Functional cardiovascular abnormalities were identified in white-coat hypertensive patients who had no identifiable structural abnormalities. Such functional abnormalities can be reversed by antihypertensive treatment. We propose that patients with white-coat hypertension might benefit from antihypertensive treatment as well as those with persistent hypertension. This hypothesis should be addressed in prospective clinical trials.
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            Time course of complete normalization of left ventricular hypertrophy during long-term antihypertensive therapy with angiotensin converting enzyme inhibitors.

            Metaanalyses have indicated that ACE inhibitors are more effective than other first-line therapies in reducing left ventricular hypertrophy (LVH). The average treatment period, however, was only approximately 6 months. The aim of the present study, therefore, was to clarify the time course and degree of reversal, and primarily to find out in how many patients a complete normalization of LVH can be achieved. Secondly, we sought to determine whether atrial enlargement can be reduced. Previously untreated hypertensive patients (mean age 46.3 +/- 9 years, eight women, 15 men) with echocardiographically confirmed LVH (left ventricular mass index ([LVMI] > 125 g/m2 for men; > 110 g/m2 for women) were prospectively treated over a 3-year treatment period with quinapril. Nine patients received 10 mg quinapril, 12 received 20 mg of quinapril daily, and five patients additionally received 25 mg hydrochlorothiazide. The time course of changes in LVMI, relative wall thickness, left atrial size, fractional shortening, and diastolic function was evaluated and ambulatory blood pressure monitoring (ABPM) and an exercise test were performed every 6 months. After a mean treatment period of only 7.5 months, there was a significant (P < .001), 17.5% decrease in LVMI with a further continuous and significant (P < .001) decrease of 38.6% after 38.3 +/- 3 months of therapy. In 90.5% of the patients a complete reversal of LVH was achieved. Fractional shortening increased significantly, the maximum being 14.6% after 38.3 +/- 3 months. The peak early/atrial velocity (E/A) ratio increased significantly (P < .01) after just 7.5 +/- 3.1 months with no further changes during follow-up. There seemed to be a parallel change with the decrease in left atrial dimension, where the most important decrease occurred after only 7.5 +/- 3.1 months (P < .01), with a further continuous reduction. Our study clearly shows that maximum reversal of LVH is a time-consuming process and that an essential goal of antihypertensive therapy should be not only a reduction in LVH but also a normalization in LV mass, left atrial size, and in diastolic dysfunction.
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              Comparison of the effects of amlodipine and diltiazem on 24-hour blood pressure, plasma catecholamines, and left ventricular mass.

              In 30 patients with mild to moderate essential hypertension and high-normal left ventricular (LV) mass, the effects of treatment for 6 months with amlodipine (5 to 10 mg every morning) versus diltiazem-sustained release (SR) (90 to 180 mg twice daily) on 24-hour blood pressure (BP), plasma catecholamines, and echocardiographic estimates of LV mass and function were evaluated. Both amlodipine and diltiazem caused stable, persistent BP reduction over 24 hours with no evidence for a "peak" effect. For a similar decrease in diastolic BP, amlodipine caused a significantly larger decrease in systolic BP. Amlodipine decreased BP by lowering total peripheral resistance, whereas diltiazem caused small decreases in both total peripheral resistance and cardiac index. Both calcium antagonists caused modest but significant decreases in supine and standing plasma catecholamines. LV wall thickness and LV mass decreased significantly over the 6 months of follow-up: -6 +/- 2 with diltiazem and -10 +/- 2 g/m2 with amlodipine. In patients taking amlodipine, the decrease in LV mass correlated significantly with the decrease in plasma norepinephrine. In contrast to rapid-acting calcium antagonists, both amlodipine and diltiazem-SR cause smooth BP control and an appropriate decrease in LV mass without activation of the sympathetic nervous system.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                1999
                February 2000
                07 March 2000
                : 92
                : 2
                : 110-114
                Affiliations
                Medical University Outpatient Division and Hypertension Clinic, University Hospital, Basel, Switzerland
                Article
                6957 Cardiology 1999;92:110–114
                10.1159/000006957
                10702653
                © 2000 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: 25, Pages: 5
                Categories
                Clinical Pharmacology

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