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      Interruption of the Progression of Heart Failure: Are ACE Inhibitors the Solution?

      Cardiology

      S. Karger AG

      Fatigue, Heart failure, Pathophysiology, ACE inhibitors, Diuretics, Dyspnea, Edema

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          Abstract

          Our options for the medical management of heart failure are aimed at preventing the development of the condition, relieving symptoms, modifying the underlying pathophysiology, and delaying or preventing disease progression. The principal symptoms of heart failure are edema, dyspnea and fatigue. Diuretics are effective in relieving edema, and dyspnea resulting from pulmonary edema. Once pulmonary edema has been treated relatively few agents are effective against residual exercise-induced dyspnea, possibly because of the numerous possible causes of this symptom. Angiotensin-converting enzyme (ACE) inhibitors have, however, been shown to improve dyspnoea by mechanisms that are not related to hemodynamic actions. These agents also improve skeletal muscle blood flow and function, thereby relieving fatigue in heart failure patients. Treatment strategies aimed at modifying the underlying pathophysiology or preventing disease progression have, with the exception of the ACE inhibitors, met with limited success. Large-scale trials have shown, however, that ACE inhibitors improve survival in patients with moderate or severe heart failure, and prevent the development of heart failure in asymptomatic patients. These agents, therefore, represent an important advance in the management of heart failure, and it is anticipated that new insights into their optimal use will follow as the mechanisms by which they exert their beneficial effects become clear.

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          Author and article information

          Journal
          CRD
          Cardiology
          10.1159/issn.0008-6312
          Cardiology
          S. Karger AG
          978-3-8055-6272-0
          978-3-318-01963-6
          0008-6312
          1421-9751
          1996
          1996
          19 November 2008
          : 87
          : Suppl 1
          : 11-15
          Affiliations
          Department of Cardiac Medicine, National Heart and Lung Hospital, London, UK
          Article
          177162 Cardiology 1996;87:11–15
          10.1159/000177162
          8681315
          © 1996 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
          Pages: 5
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