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      Early Use of Beta-Blockers Is Associated with Attenuation of Serum C-Reactive Protein Elevation and Favorable Short-Term Prognosis after Acute Myocardial Infarction

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          Abstract

          Background: We have reported that a marked elevation in serum C-reactive protein (CRP) level is a predictor for infarct expansion and cardiac rupture after AMI. Although β-blockers prevent cardiac rupture after AMI, their effect on serum CRP elevation has not been determined. Methods: We studied a total of 154 patients with first Q-wave AMI. Patients complicated by pump failure were excluded from this study. Eighty-two patients received β-blocker treatment within 24 h of the onset of AMI, while 72 patients received no β-blocker treatment. Peak serum creatine kinase (CK) and CRP levels were determined by serial measurements. Results: There was no difference between the groups according to age, sex, coronary risk factors, pre-infarction angina, infarct site, prior use of cardiovascular drugs, use of revascularization therapy, and prevalence of multivessel disease. β-Blocker treatment was associated with a lower peak CRP level (6.9 ± 6.1 vs.10.8 ± 9.3 mg/dl, p = 0.002), a shorter duration from the onset to the peak CRP level (2 ± 1 vs. 3 ± 2 days, p < 0.0001), a lower incidence of cardiac rupture (p = 0.03) and lower in-hospital cardiac mortality (p = 0.02), despite similar peak CK levels. Conclusion: The early use of β-blockers is associated with decreased serum CRP level and a favorable clinical outcome after first Q-wave AMI, suggesting some beneficial effects of β-blockers on infarct healing after AMI.

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          Most cited references 6

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          Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial

          (2001)
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            Effect of beta-blockers on circulating levels of inflammatory and anti-inflammatory cytokines in patients with dilated cardiomyopathy.

            This study was designed to evaluate the beneficial effect of beta-blockers on circulating cytokine levels in patients with dilated cardiomyopathy (DCM). Elevated circulating levels of inflammatory cytokines have been reported in patients with DCM. However, alterations of the levels of inflammatory and anti-inflammatory cytokines in association with beta-blocker therapy are unknown. We studied 32 patients with idiopathic DCM who had been treated with digitalis, diuretics and angiotensin-converting enzyme inhibitors. In addition to this combination therapy, beta-blockers were started in all patients. Serum levels of interleukin (IL)-10, tumor necrosis factor-alpha (TNF-alpha) and soluble TNF receptors (sTNF-R1 and R2) were measured at baseline and 12 weeks after the initiation of beta-blocker therapy. We also measured plasma levels of neurohumoral factors, as well as left ventricular (LV) size and function. Ten age-matched subjects with no cardiac disease served as the control group. Baseline levels of IL-10, TNF-alpha and sTNF-R2 were significantly higher in patients with DCM than in control subjects (p < 0.05). There was a significant positive correlation between IL-10 and TNF-alpha levels (r = 0.545, p = 0.029). The TNF-alpha/IL-10 ratio correlated well with plasma epinephrine levels (r = 0.677, p = 0.025), and the level of sTNF-R2 was closely related to LV size. Serum levels of IL-10, TNF-alpha and sTNF-R2 were significantly decreased during beta-blocker therapy (p < 0.005). Our findings indicate that beta-blockers have an important immunoregulatory role in modifying the dysregulated cytokine network in DCM. This effect of beta-blockers may be partly responsible for the efficacy of therapeutic drugs for heart failure.
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              Effect of metoprolol on cytokine levels in chronic heart failure--a substudy in the Metoprolol Controlled-Release Randomised Intervention Trial in Heart Failure (MERIT-HF).

              Enhanced immune activation has been suggested to be involved in the pathogenesis of congestive heart failure (CHF). There is evidence for interactions between the sympathetic nervous system and the immune system. We therefore examined the effect of the selective beta(1)-receptor blocker metoprolol on various immunologic variables in CHF. Eighty-one patients with CHF were randomized to metoprolol or placebo in a double-blind trial. Plasma levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-10, soluble IL-2 receptor (sIL-2R), monocyte chemoattractant peptide-1, and IL-8 were measured at baseline, after 3 months, and at the end of the study (11.4 +/- 0.4 months). Our main findings were (1) at baseline TNF-alpha, IL-6, IL-8, monocyte chemoattractant peptide-1, and sIL-2R but not IL-10 levels were markedly elevated in patients with CHF compared with controls; (2) during treatment with metoprolol, but not with placebo, there was a significant decrease in sIL-2R after 3 months, with a return to baseline at the end of the study; and (3) levels of all other immunologic variables remained unchanged throughout the study in both the metoprolol and the placebo groups. Our findings suggest that metoprolol treatment in CHF is associated with a significant but temporary decrease in sIL-2R, possibly reflecting down-modulation of T-cell activation. However, an enhanced immune activation also persisted in the metoprolol group, suggesting a potential for more specific immunomodulatory therapy in CHF.
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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
                February 2003
                24 February 2003
                : 99
                : 1
                : 47-53
                Affiliations
                Cardiopulmonary Division, Department of Medicine, Keio University School of Medicine, Tokyo, Japan
                Article
                68449 Cardiology 2003;99:47–53
                10.1159/000068449
                12589122
                © 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: 1, Tables: 4, References: 33, Pages: 7
                Categories
                Coronary Care

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