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      Amlodipine: Effective for Treatment of Mild to Moderate Essential Hypertension and Left Ventricular Hypertrophy

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          Abstract

          This was a 20-week, open-label, uncontrolled clinical investigation of the long-acting calcium antagonist amlodipine in 33 male or female patients with essential hypertension and left ventricular hypertrophy (LVH). A once-daily dose (5–10 mg/day) of amlodipine provided a consistent antihypertensive effect, reducing the sitting diastolic (–13.8% change) and systolic (–13.0% change) blood pressures by clinically meaningful and statistically significant (p = 0.0001, n = 33) amounts. Amlodipine had no effect on heart rate. A significant regression in LVH was seen (left ventricular mass index reduced from 169.0 [SD 30.7] g/m<sup>2</sup> to 140.6 [SD 19.6] g/m<sup>2</sup>, p < 0.01, n = 12). There was also a significant reduction in total peripheral resistance and improvement in left ventricular diastolic filling (E/A ratio increased from 0.86 pre-treatment to 1.03 post-treatment, p = 0.038, n = 12). These results are consistent with other studies in showing that a relatively short treatment regimen with amlodipine is associated with a significant reduction in left ventricular mass index.

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          Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings.

          Richard Devereux, Daniel R. Alonso, Elizabeth M. Lutas … (1986)
          To determine the accuracy of echocardiographic left ventricular (LV) dimension and mass measurements for detection and quantification of LV hypertrophy, results of blindly read antemortem echocardiograms were compared with LV mass measurements made at necropsy in 55 patients. LV mass was calculated using M-mode LV measurements by Penn and American Society of Echocardiography (ASE) conventions and cube function and volume correction formulas in 52 patients. Penn-cube LV mass correlated closely with necropsy LV mass (r = 0.92, p less than 0.001) and overestimated it by only 6%; sensitivity in 18 patients with LV hypertrophy (necropsy LV mass more than 215 g) was 100% (18 of 18 patients) and specificity was 86% (29 of 34 patients). ASE-cube LV mass correlated similarly to necropsy LV mass (r = 0.90, p less than 0.001), but systematically overestimated it (by a mean of 25%); the overestimation could be corrected by the equation: LV mass = 0.80 (ASE-cube LV mass) + 0.6 g. Use of ASE measurements in the volume correction formula systematically underestimated necropsy LV mass (by a mean of 30%). In a subset of 9 patients, 3 of whom had technically inadequate M-mode echocardiograms, 2-dimensional echocardiographic (echo) LV mass by 2 methods was also significantly related to necropsy LV mass (r = 0.68, p less than 0.05 and r = 0.82, p less than 0.01). Among other indexes of LV anatomy, only measurement of myocardial cross-sectional area was acceptably accurate for quantitation of LV mass (r = 0.80, p less than 0.001) or diagnosis of LV hypertrophy (sensitivity = 72%, specificity = 94%).(ABSTRACT TRUNCATED AT 250 WORDS)
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            Reversal of left ventricular hypertrophy in essential hypertension. A meta-analysis of randomized double-blind studies.

            Roland E Schmieder, P. Martus, David Klingbeil (1996)
            To determine the ability of various antihypertensive agents to reduce left ventricular hypertrophy, a strong, blood pressure-independent cardiovascular risk factor, in persons with essential hypertension. MEDLINE, DIMDI, RINGDOC, ADES, EMBASE, and review articles through July 1995 (English-language and full articles only). Meta-analysis of all published articles including only double-blind, randomized, controlled clinical studies with parallel-group design. Intensive literature search and data extraction according to a prefixed scheme performed independently by 2 investigators. Reduction of left ventricular mass index after antihypertensive therapy with placebos, diuretics, beta-blockers, calcium channel blockers, or angiotensin-converting enzyme (ACE) inhibitors was the principal parameter. Of 471 identified references describing the effects of antihypertensive drugs on left ventricular hypertrophy, only 39 clinical trials fulfilled the inclusion criteria of our study. We found that the decrease in left ventricular mass index was more marked the greater was the decline in blood pressure (systolic r=0.46, P<.001; diastolic r=0.21, P=.08) and the longer was the duration of therapy (r=0.38, P<.01). After adjustment for different durations of treatment (mean duration of treatment, 25 weeks), left ventricular mass decreased 13% with ACE inhibitors, 9% with calcium channel blockers, 6% with beta-blockers, and 7% with diuretics. There was a significant difference between drug classes (P<.01): ACE inhibitors reduced left ventricular mass more than beta-blockers (significant, P<.05) and diuretics (tendency, P=.08). Similar differences between drug classes were found with regard to effect on left ventricular wall thickness (P<.05). The database of articles published through July 1995 is small and incomplete, and most of the articles are of poor scientific quality. In this first meta-analysis including only double-blind, randomized, controlled clinical studies, decline in blood pressure, duration of drug treatment, and drug class determined the reductions in left ventricular mass index. The ACE inhibitors seemed to be more potent than beta-blockers and diuretics in the reduction of left ventricular mass index; calcium channel blockers were somewhat in the intermediate range. The ACE inhibitors and, to a lesser extent, calcium channel blockers emerged as first-line candidates to reduce the risk associated with left ventricular hypertrophy.
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              Comparison of the effects of amlodipine and diltiazem on 24-hour blood pressure, plasma catecholamines, and left ventricular mass.

              F Leenen, MD, PhD (1996)
              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
                Journal ID (publisher-id): CRD
                Journal ID (nlm-ta): Cardiology
                Journal ID (doi): 10.1159/issn.0008-6312
                Title: Cardiology
                Publisher: S. Karger AG
                ISBN: 978-3-8055-7309-2
                ISBN: 978-3-318-00774-9
                ISSN (Print): 0008-6312
                ISSN (Electronic): 1421-9751
                Publication date Subscription-year: 2001
                Publication date (Print): 2001
                Publication date (Electronic): 08 November 2001
                Volume: 96
                Issue: Suppl 1
                Pages: 10-18
                Affiliations
                aUniversity Department of Cardiovascular Medicine, City Hospital NHS Trust, Birmingham, and bWordesley Hospital, Stourbridge, UK
                Article
                Publisher ID: 49096 Other ID: Cardiology 2001;96(suppl 1):10–18
                DOI: 10.1159/000049096
                PubMed ID: 11574741
                SO-VID: e31e91d7-71ec-4dc9-9b0c-1da61e6eca78
                Copyright © © 2001 S. Karger AG, Basel
                License:

                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.

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                Page count
                Figures: 4, Tables: 5, References: 47, Pages: 9
                Categories
                Subject: Paper

                ScienceOpen disciplines: General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Keywords: Amlodipine,Essential hypertension,Left ventricular hypertrophy
                Data availability:
                ScienceOpen disciplines: General medicine, Neurology, Cardiovascular Medicine, Internal medicine, Nephrology
                Keywords: Amlodipine, Essential hypertension, Left ventricular hypertrophy

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