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      Dietary Intake of Various Nutrients in Older Patients with Congestive Heart Failure

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          Abstract

          Background and Aims: Anorexia, nausea and premature satiety with eating, prevalent in congestive heart failure (CHF), have been held responsible for reduced dietary intake and deficiency of magnesium, potassium and probably other nutrients. Since solid data is not available, this study was undertaken with the following aims (1) to assess dietary intake in CHF, (2) to compare dietary intake in older CHF patients with a similar patient population free of CHF (control group), and (3) to evaluate these data in patients with moderate versus severe CHF. Methods and Results: Dietary intake of 57 consecutively hospitalized furosemide-treated CHF patients over the age of 60 was compared with that of 40 similar patients free of CHF. In addition, a statistical analysis was performed comparing the data of the 37 patients with moderate versus the 20 patients with severe CHF. Dietary content of various nutrients was assessed with the food frequency recall technique. Dietary intake was comparable in the two respective pairs of groups. However, the intake of magnesium, calcium, zinc, copper, manganese, energy, thiamin, riboflavin, and folate in all subgroups fell short of recommended levels for intake, while vitamins A, C and niacin contents exceeded those recommended. Intakes of potassium andproteins were within the recommended values. Conclusions: CHF per se, even severe CHF, is not responsible for a reduced dietary intake of various nutrients. A population-related dietary culture, old age or other chronic conditions, rather than CHF, might be mainly involved. The increased intake of vitamins A, C and niacin in our patients may be attributed to the high content of fruits and vegetables in the Mediterranean diet. Insufficient intake of the above-mentioned group of electrolytes and essential nutrients may contribute to the frequently observed negative balance of some of them. This is especially relevant in furosemide-treated CHF patients. Therefore, supplementation should be considered.

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          Insights into the pathogenesis of chronic heart failure: immune activation and cachexia.

          Body wasting, i.e, cardiac cachexia, is a complication of chronic heart failure (CHF). The authors have suggested that cardiac cachexia should be diagnosed when nonedematous weight loss of more than 7.5% of the premorbid normal weight occurs over a time period of more than 6 months. In an unselected CHF outpatient population, 16% of patients were found to be cachectic. The cachectic state is predictive of poor survival independently of age, functional class, ejection fraction, and exercise capacity. Patients with cardiac cachexia suffer from a general loss of fat, lean, and bone tissue. Cachectic CHF patients are weaker and fatigue earlier. The pathophysiologic causes of body wasting in patients with CHF remain unclear, but initial studies have suggested that humoral neuroendocrine and immunologic abnormalities may be of importance. Cachectic CHF patients show increased plasma levels of catecholamines, cortisol, and aldosterone. Several studies have shown that cardiac cachexia is linked to increased plasma levels of tumor necrosis factor alpha. The degree of body wasting is strongly correlated with neurohormonal and immune abnormalities. Some investigators have suggested that endotoxin may be important in triggering immune activation in CHF patients. Available studies suggest that cardiac cachexia is a multifactorial neuroendocrine and immunologic disorder that carries a poor prognosis. A complex catabolic-anabolic imbalance in different body systems may cause body wasting in patients with CHF.
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            Thiamin status, diuretic medications, and the management of congestive heart failure.

            To assess the prevalence of thiamin deficiency in patients with congestive heart failure who are treated with diuretics that inhibit sodium and chloride reabsorption in the thick ascending limb of the loop of Henle (loop diuretic therapy). A cross-sectional investigation of thiamin status of consecutive patients with congestive heart failure being treated with loop diuretic therapy. Cardiology clinic of a midwestern tertiary-care medical center. Thirty-eight patients were recruited (mean age +/- standard deviation = 55 +/- 14 years). Validation of methodology was conducted with nine age-matched control subjects. Thiamin status was assessed biochemically by in vitro erythrocyte transketolase activity assay. Assessment of dietary intake of thiamin was accomplished with a semiquantitative food frequency questionnaire. Fisher's exact test and logistic regression were used to evaluate relationships between thiamin status and variables of interest. Biochemical evidence of thiamin deficiency was found in 8 of 38 (21%) patients. Evidence of risk for dietary thiamin inadequacy was found in 10 of 38 patients (25%). Seven of the 8 patients with biochemical evidence of thiamin deficiency met study criteria for dietary adequacy, although quantified data suggested that only 4 of the patients achieved two thirds of the Recommended Dietary Allowance. Biochemical evidence of thiamin deficiency tended to be more common among patients with poor left ventricular ejection fractions (P = .07). Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk.
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              Author and article information

              Journal
              CRD
              Cardiology
              10.1159/issn.0008-6312
              Cardiology
              S. Karger AG
              0008-6312
              1421-9751
              2003
              July 2003
              10 July 2003
              : 99
              : 4
              : 177-181
              Affiliations
              aDepartment of Internal Medicine ‘F’ and bDietary and Nutrition Unit, Assaf Harofeh Medical Center (affiliated to Sackler School of Medicine, Tel Aviv University), Zerifin, Israel
              Article
              71246 Cardiology 2003;99:177–181
              10.1159/000071246
              12845243
              © 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: 2, References: 22, Pages: 5
              Categories
              General Cardiology

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