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      Exercise-Induced Increase in Lipid Peroxidation in Patients with Chronic Heart Failure: Relation to Exercise Intolerance

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          Abstract

          Background: Little is known about the relationship between exercise intolerance and lipid peroxidation in chronic heart failure (CHF) patients. This study was designed to investigate the relationship between exercise-induced plasma malondialdehyde (MDA) changes in CHF patients and to determine whether there is any association between plasma MDA levels and exercise capacity assessed by cardiopulmonary exercise testing. Methods: Cardiopulmonary exercise testing was applied to 31 CHF patients (16 ischemic, 15 idiopathic) and controls. Rest and peak exercise blood samples were analyzed for MDA. Results: Patients with CHF had elevation of plasma MDA levels during exercise compared with controls (p < 0.001 vs. p = 0.588). MDA change remained significant both in ischemic and idiopathic cardiomyopathy groups (p < 0.05 and p < 0.01, respectively). ΔMDA (peak exercise MDA – rest MDA) showed significant inverse correlation with peak oxygen consumption in patients with CHF. Conclusion: Lipid peroxidation is increased in patients with CHF during exercise regardless of etiology, and this increase is inversely related to oxygen consumption.

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          Most cited references 17

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          Reactive oxygen species in the vasculature: molecular and cellular mechanisms.

          Accumulating evidence indicates that reactive oxygen species (ROS) play major roles in the initiation and progression of cardiovascular dysfunction associated with diseases such as hyperlipidemia, diabetes mellitus, hypertension, ischemic heart disease, and chronic heart failure. ROS produced by migrating inflammatory cells as well as vascular cells (endothelial cells, vascular smooth muscle cells, and adventitial fibroblasts) have distinct functional effects on each cell type. These include cell growth, apoptosis, migration, inflammatory gene expression, and matrix regulation. ROS, by regulating vascular cell function, can play a central role in normal vascular physiology, and can contribute substantially to the development of vascular disease.
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            Oxygen, oxidative stress, hypoxia, and heart failure

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              Oxygen free radicals and congestive heart failure.

              Plasma lipid peroxides (malondialdehyde) and thiols were measured in 45 patients with congestive heart failure and 45 controls. Malondialdehyde concentrations were significantly higher in the patients with congestive heart failure (median 9.0 nmol/ml interquartile range (IQR) 7.9-10.2) than in the controls (median 7.7 nmol/ml (IQR 6.9-9.2)). Plasma thiols were significantly lower in congestive heart failure (median 420 mumol/l (IQR 379-480)) than in the controls (median 463 mumol/l (IQR 445-525)). There was a significant but weak negative correlation between malondialdehyde and left ventricular ejection fraction (r = -0.35) and a positive correlation between plasma thiols and left ventricular ejection fraction (r = 0.39). This study provides clinical support for experimental data indicating that free radicals may be important in heart failure. It also suggests that the degree of free radical production may be linked to the severity of the disease.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2007
                November 2007
                09 February 2007
                : 108
                : 4
                : 307-313
                Affiliations
                aDepartment of Cardiology, Siyami Ersek Cardiovascular Research and Training Hospital, bGenlab Medical Diagnostics and Research Laboratory, and cDepartment of Chemical Engineering, Faculty of Engineering, Marmara University, Istanbul, Turkey
                Article
                99100 Cardiology 2007;108:307–313
                10.1159/000099100
                17290101
                © 2007 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
                Figures: 3, Tables: 2, References: 30, Pages: 7
                Categories
                Original Research

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