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      Functional Capacity Impairment in Patients with Coronary Artery Disease: Prevalence, Risk Factors and Prognosis

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          Abstract

          Background: Some patients developing heart failure and functional capacity impairment have no history of myocardial infarction (MI), and stable angina pectoris is their principal clinical manifestation of coronary artery disease (CAD). The present study was aimed to evaluate the outcome of CAD-related functional capacity impairment in patients with and without a history of MI over a 7.7-year follow-up. Methods: The study sample comprised 14,283 coronary patients aged 45–74 years, screened for participation in the Bezafibrate Infarction Prevention study. The presence of NYHA functional class II was defined as mild functional capacity impairment and the presence of NYHA functional class III–IV was defined as advanced functional capacity impairment. Results: The patients were divided in two groups: (1) those with a history of MI, 10,307 patients, who formed three subgroups: NYHA I 7,551 patients (73.3%); NYHA II 2,176 patients (21.1%); NYHA III + IV 580 patients (5.6%), and (2) those without a history of MI, 3,976 patients, who also formed three subgroups: NYHA I 2,744 patients (69.0%); NYHA 981 patients (24.7%); NYHA III + IV 251 patients (6.3%). Multivariate analysis identified a history of MI as a consistent predictor of increased all-cause and cardiac mortality for patients with NYHA I, II and III + IV subgroups with escalating significance for patients with advanced functional capacity impairment: hazard ratios of 1.55 (95% CI 1.36–1.75), 1.56 (95% CI 1.30–1.86) and 1.72 (95% CI 1.24–2.40) for all-cause and 1.93 (95% CI 1.60–2.33), 1.73 (95% 1.35–2.20) and 3.22 (95% CI 1.87–5.54) for cardiac mortality, respectively. Conclusions: The prevalence of low functional capacity is similar among coronary patients with and without a history of MI, but their long-term survival differs substantially in favor of the latter. Therefore, two different types of CAD-related advanced functional capacity impairments (post-MI and non-post-MI) can be distinguished.

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          Most cited references 18

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          Apoptosis in the failing human heart.

           R. Reed,  E Quaini,  P Anversa (1997)
          Loss of myocytes is an important mechanism in the development of cardiac failure of either ischemic or nonischemic origin. However, whether programmed cell death (apoptosis) is implicated in the terminal stages of heart failure is not known. We therefore studied the magnitude of myocyte apoptosis in patients with intractable congestive heart failure. Myocardial samples were obtained from the hearts of 36 patients who underwent cardiac transplantation and from the hearts of 3 patients who died soon after myocardial infarction. Samples from 11 normal hearts were used as controls. Apoptosis was evaluated histochemically, biochemically, and by a combination of histochemical analysis and confocal microscopy. The expression of two proto-oncogenes that influence apoptosis, BCL2 and BAX, was also determined. Heart failure was characterized morphologically by a 232-fold increase in myocyte apoptosis and biochemically by DNA laddering (an indicator of apoptosis). The histochemical demonstration of DNA-strand breaks in myocyte nuclei was coupled with the documentation of chromatin condensation and fragmentation by confocal microscopy. All these findings reflect apoptosis of myocytes. The percentage of myocytes labeled with BCL2 (which protects cells against apoptosis) was 1.8 times as high in the hearts of patients with cardiac failure as in the normal hearts, whereas labeling with BAX (which promotes apoptosis) remained constant. The near doubling of the expression of BCL2 in the cardiac tissue of patients with heart failure was confirmed by Western blotting. Programmed death of myocytes occurs in the decompensated human heart in spite of the enhanced expression of BCL2; this phenomenon may contribute to the progression of cardiac dysfunction.
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            Risk Factors for Congestive Heart Failure in US Men and Women

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              • Article: not found

              The heart failure epidemic: exactly how big is it?

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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
                December 2003
                16 January 2004
                : 100
                : 4
                : 207-215
                Affiliations
                aCardiac Rehabilitation Institute and bBezafibrate Infarction Prevention Study Coordinating Center, NeufeldCardiacResearch Institute, Chaim Sheba Medical Center, Tel-Hashomer, affiliated with Sackler Faculty of Medicine, Tel-AvivUniversity, Tel-Aviv, Israel
                Article
                74814 Cardiology 2003;100:207–215
                10.1159/000074814
                14713732
                © 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
                Figures: 2, Tables: 5, References: 47, Pages: 9
                Categories
                General Cardiology

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