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      Heart Failure in Diabetes mellitus: Clinical Features and Prognostic Implications

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          Abstract

          We defined the prevalence and impact on survival of clinical bedside variables in 385 patients with symptomatic congestive heart failure (CHF), of whom there were 176 with and 209 without diabetes mellitus. Patients were consecutively hospitalized and admitted for various acute conditions. Following discharge all-cause mortality was recorded. Prevalence and association of various variables with mortality were statistically analyzed. Prevailing in the diabetics versus nondiabetics were younger age (p < 0.05), pulmonary edema on admission (p = 0.002), using furosemide >80 mg/day (p < 0.01) for >1 year (p < 0.01) and hyponatremia (p = 0.01). Less prevalent were chronic lung disease (p < 0.01) and cardiac arrhythmias (p = 0.001). On follow-up extending up to 60 months, diabetic patients, especially those with fasting blood glucose levels on admission ≧180 mg/dl, survived for a shorter period of time than nondiabetics (p = 0.02). Associated with increased mortality in the diabetic group were female gender (p = 0.04), furosemide ≧80 mg/day (p < 0.001) and renal dysfunction (RD; p = 0.04). The respective variables in the nondiabetics were advanced age (p < 0.001) and RD (p = 0.002). Although they were younger, diabetic patients presented more severe CHF. It is recommended that special attention should be given to diabetic females, those using higher furosemide dosages and those suffering from RD.

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          Most cited references 20

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          The prognostic implications of renal insufficiency in asymptomatic and symptomatic patients with left ventricular systolic dysfunction.

          The present analysis examines the prognostic implications of moderate renal insufficiency in patients with asymptomatic and symptomatic left ventricular systolic dysfunction. Chronic elevations in intracardiac filling pressures may lead to progressive ventricular dilation and heart failure progression. The ability to maintain fluid balance and prevent increased intracardiac filling pressures is critically dependent on the adequacy of renal function. This is a retrospective analysis of the Studies of Left Ventricular Dysfunction (SOLVD) Trials, in which moderate renal insufficiency is defined as a baseline creatinine clearance <60 ml/min, as estimated from the Cockroft-Gault equation. In the SOLVD Prevention Trial, multivariate analyses demonstrated moderate renal insufficiency to be associated with an increased risk for all-cause mortality (Relative Risk [RR] 1.41; p = 0.001), largely explained by an increased risk for pump-failure death (RR 1.68; p = 0.007) and the combined end point death or hospitalization for heart failure (RR 1.33; p = 0.001). Likewise, in the Treatment Trial, multivariate analyses demonstrated moderate renal insufficiency to be associated with an increased risk for all-cause mortality (RR 1.41; p = 0.001), also largely explained by an increased risk for pump-failure death (RR 1.49; p = 0.007) and the combined end point death or hospitalization for heart failure (RR 1.45; p = 0.001). Even moderate degrees of renal insufficiency are independently associated with an increased risk for all-cause mortality in patients with heart failure, largely explained by an increased risk of heart failure progression. These data suggest that, rather than simply being a marker of the severity of underlying disease, the adequacy of renal function may be a primary determinant of compensation in patients with heart failure, and therapy capable of improving renal function may delay disease progression.
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            Congestive Heart Failure in Type 2 Diabetes: Prevalence, incidence, and risk factors

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              Heart failure: the frequent, forgotten, and often fatal complication of diabetes.

               D. S.H. Bell (2003)
              There is a high frequency of heart failure (HF) accompanied by an increased mortality risk for patients with diabetes. The poor prognosis of these patients has been explained by an underlying diabetic cardiomyopathy exacerbated by hypertension and ischemic heart disease. In these patients, activation of the sympathetic nervous system results in increased myocardial utilization of fatty acids and induction of fetal gene programs, decreasing myocardial function. Activation of the renin-angiotensin system results in myocardial remodeling. It is imperative for physicians to intercede early to stop the progression of HF, yet at least half of patients with left ventricular dysfunction remain undiagnosed and untreated until advanced disease causes disability. This delay is largely because of the asymptomatic nature of early HF, which necessitates more aggressive assessment of HF risk factors and early clinical signs. Utilization of beta-blockade, ACE inhibitors, or possibly angiotensin receptor blockers is essential in preventing remodeling with its associated decline in ventricular function. beta-Blockers not only prevent, but may also reverse, cardiac remodeling. Glycemic control may also play an important role in the therapy of diabetic HF. The adverse metabolic side effects that have been associated with beta-adrenergic inhibitors in the diabetic patient may be circumvented by use of a third-generation beta-blocker. Prophylactic utilization of ACE inhibitors and beta-blockers to avoid, rather than await, the need to treat HF should be considered in high-risk diabetic patients.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2005
                April 2005
                07 April 2005
                : 103
                : 3
                : 161-166
                Affiliations
                Department of Internal Medicine ‘F’, Assaf Harofeh Medical Center (affiliated to Sackler School of Medicine, Tel Aviv University), Zerifin, Israel
                Article
                84587 Cardiology 2005;103:161–166
                10.1159/000084587
                15785022
                © 2005 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: 1, Tables: 2, References: 29, Pages: 6
                Categories
                General Cardiology

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