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      Long-Term Outcome of Intravenous Magnesium Therapy in Thrombolysis-Ineligible Acute Myocardial Infarction Patients

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          Abstract

          The aim of our study was to analyze the long-term survival and cardiac function in 194 consecutive, thrombolysis-ineligible acute myocardial infarction (AMI) patients receiving 48-hour intravenous magnesium sulfate (22 g) – 96 patients, compared with placebo – 98 patients. After a mean 4.8-year follow-up, all-cause mortality and cardiac mortality were significantly lower in the magnesium compared to the placebo group [(18 vs. 33 patients, p < 0.01) and (12 vs. 30 patients, p < 0.001), respectively]. Rest radionuclide ventriculography tests for left-ventricular ejection fraction (LVEF) were assessed in surviving patients up to completion of follow-up. Magnesium-treated patients had a significantly higher LVEF (0.51 ± 0.10 vs. 0.44 ± 0.14, p < 0.05) and a lower incidence of heart failure compared to placebo-treated patients (12 vs. 3 patients, p = 0.02). Beneficial effects of intravenous magnesium therapy in thrombolysis-ineligible AMI patients appeared to last for at least 4.8 years, concomitant with preserved LVEF, suggesting a favorable role for acute magnesium treatment in these patients.

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          Most cited references12

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          ISIS-4: A randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58 050 patients with suspected acute myocardial infarction

          (1995)
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            Practice variation and missed opportunities for reperfusion in ST-segment-elevation myocardial infarction: findings from the Global Registry of Acute Coronary Events (GRACE).

            The benefits of reperfusion therapy for patients with acute coronary syndromes have been established, but there is much variation in the type of reperfusion given and decisions about which patients are eligible. This study assessed current practices in relation to reperfusion therapy of ST-segment-elevation myocardial infarction from data collected in the multinational, prospective Global Registry of Acute Coronary Events. 94 hospitals in 14 countries are recruiting patients for the registry. Hospitals are organised into population-based clusters that reflect the population characteristics of the region. Information about patients' demographic characteristics, presenting symptoms, medical history, time between symptom onset and presentation, and clinical and electrocardiographic features is recorded in a standard case record. Of the 9251 patients enrolled, 1763 presented within 12 h of symptom onset with ST-segment-elevation myocardial infarction. Of these, 30% did not receive reperfusion therapy. Elderly patients (75 years and older), those presenting without chest pain, and those with a history of diabetes, congestive heart failure, myocardial infarction, or coronary bypass surgery were less likely to receive reperfusion therapy. The rate of primary percutaneous coronary intervention was highest in the USA and lowest in Australia, New Zealand, and Canada. The rate at sites with a catheterisation laboratory was 19% compared with zero at sites without this facility. A substantial proportion of patients who are eligible for reperfusion therapy still do not receive this treatment. These typically high-risk patients can be identified in advance, and reasons for the underuse of these beneficial treatments need to be clarified.
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              Magnesium deficiency in vitro enhances free radical-induced intracellular oxidation and cytotoxicity in endothelial cells.

              The effect of magnesium (Mg)-deficient culture on endothelial cell susceptibility to oxidative stress was examined. Bovine endothelial cells were cultured in either control sufficient (0.8 mM) or deficient (0.4 mM) levels of MgCl2. Oxygen radicals were produced extracellularly by the addition of dihydroxyfumarate and Fe(3+)-ADP. Isolated Mg-deficient endothelial cells produced 2- to 3-fold higher levels of thiobarbituric acid (TBA)-reactive materials when incubated with this free radical system. Additional studies were performed using digitized video microscopy and 2',7'-dichlorofluorescein diacetate (DCFDA) as an intracellular indicator for oxidative events at the single cell level. In response to the exogenous oxidative stress, endothelial cells exhibited a time-dependent increase in fluorescence, suggestive of intracellular lipid peroxidation. The increase in cellular fluorescence began within 1 min of free radical addition; the Mg-deficient cells exhibited a more rapid increase in fluorescence than that of Mg-sufficient cells. In separate experiments, cellular viability was assessed using the Trypan blue exclusion assay. Mg deficiency increased cytotoxicity of the added oxyradicals, but the loss of cellular viability began to occur only after 15 min of free radical exposure, lagging behind the detection of intracellular oxidation products. These results suggest that increased oxidative endothelial cell injury may contribute to vascular injury during Mg deficiency.
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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
                : 205-210
                Affiliations
                Heart Institute, Sheba Medical Center, Tel-Hashomer and Sackler School of Medicine, Tel-Aviv University, Tel Hashomer, Israel
                Article
                71250 Cardiology 2003;99:205–210
                10.1159/000071250
                12845247
                251431cc-b741-4a68-a53e-d2668a32a1a8
                © 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.

                History
                : 16 December 2002
                : 08 April 2003
                Page count
                Figures: 1, Tables: 2, References: 34, Pages: 6
                Categories
                Coronary Care

                General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Myocardial infarction,Clinical trials,Mortality,Magnesium,Coronary disease

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