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      Effect of Renal Failure on Peak Troponin Ic Level in Patients with Acute Myocardial Infarction

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          Abstract

          Objectives: Peak troponin Ic (cTnI) level could be influenced by renal function. We evaluated the effect of moderate to severe renal failure on peak cTnI level during acute myocardial infarction (AMI). Methods: One hundred and twenty-five consecutive patients admitted to the coronary care unit of a university hospital in France for primary angioplasty during AMI were retrospectively studied. Results: The correlations between peak cTnI level, peak creatine phosphokinase (CK) level, peak cTnI/peak CK ratio and creatinine clearance (CrCl) were assessed. The peak cTnI/peak CK ratio was considered in order to standardize the peak cTnI level with the extent of myocardial necrosis. There was no significant correlation between CrCl and peak CK (r = 0.01, p = 0.95), peak cTnI (r = –0.08, p = 0.38) or the peak cTnI/peak CK ratio (r = –0.14, p = 0.13). There was a trend towards higher peak cTnI in patients with moderate to severe renal failure. The peak cTnI/peak CK ratio did not significantly differ among patients according to CrCl stratification, whereas the ratio of log-transformed values was significantly higher in patients with moderate to severe renal failure. Conclusion: In patients with AMI, the peak cTnI level seemed to be influenced by renal function.

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          Most cited references 12

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          Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes.

          In patients with acute coronary syndromes, it is desirable to identify a sensitive serum marker that is closely related to the degree of myocardial damage, provides prognostic information, and can be measured rapidly. We studied the prognostic value of cardiac troponin I levels in patients with unstable angina or non-Q-wave myocardial infarction. In a multicenter study, blood specimens from 1404 symptomatic patients were analyzed for cardiac troponin I, a serum marker not detected in the blood of healthy persons. The relation between mortality at 42 days and the level of cardiac troponin I in the specimen obtained on enrollment was determined both before and after adjustment for baseline characteristics. The mortality rate at 42 days was significantly higher in the 573 patients with cardiac troponin I levels of at least 0.4 ng per milliliter (21 deaths, or 3.7 percent) than in the 831 patients with cardiac troponin I levels below 0.4 ng per milliliter (8 deaths, or 1.0 percent; P or = 65 years). In patients with acute coronary syndromes, cardiac troponin I levels provide useful prognostic information and permit the early identification of patients with an increased risk of death.
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            Troponin T levels in patients with acute coronary syndromes, with or without renal dysfunction.

            Among patients with suspected acute coronary syndromes, cardiac troponin T levels have prognostic value. However, there is concern that renal dysfunction may impair the prognostic value, because cardiac troponin T may be cleared by the kidney. We analyzed the outcomes in 7033 patients enrolled in the Global Use of Strategies to Open Occluded Coronary Arteries IV trial who had complete base-line data on troponin T levels and creatinine clearance rates. The troponin T level was considered abnormal if it was 0.1 ng per milliliter or higher, and creatinine clearance was assessed in quartiles. The primary end point was a composite of death or myocardial infarction within 30 days. Death or myocardial infarction occurred in 581 patients. Among patients with a creatinine clearance above the 25th percentile value of 58.4 ml per minute, an abnormally elevated troponin T level was predictive of an increased risk of myocardial infarction or death (7 percent vs. 5 percent; adjusted odds ratio, 1.7; 95 percent confidence interval, 1.3 to 2.2; P<0.001). Among patients with a creatinine clearance in the lowest quartile, an elevated troponin T level was similarly predictive of increased risk (20 percent vs. 9 percent; adjusted odds ratio, 2.5; 95 percent confidence interval, 1.8 to 3.3; P<0.001). When the creatinine clearance rate was considered as a continuous variable and age, sex, ST-segment depression, heart failure, previous revascularization, diabetes mellitus, and other confounders had been accounted for, elevation of the troponin T level was independently predictive of risk across the entire spectrum of renal function. Cardiac troponin T levels predict short-term prognosis in patients with acute coronary syndromes regardless of their level of creatinine clearance.
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              Skeletal muscle dysfunction in chronic renal failure: effects of exercise.

              A number of chronic illnesses such as renal failure (CRF), obstructive pulmonary disease, and congestive heart failure result in a significant decrease in exercise tolerance. There is an increasing awareness that prescribed exercise, designed to restore some level of physical performance and quality of life, can be beneficial in these conditions. In CRF patients, muscle function can be affected by a number of direct and indirect mechanisms caused by renal disease as well as various treatment modalities. The aims of this review are twofold: first, to briefly discuss the mechanisms by which CRF negatively impacts skeletal muscle and, therefore, exercise capacity, and, second, to discuss the available data on the effects of programmed exercise on muscle function, exercise capacity, and various other parameters in CRF.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2008
                March 2008
                17 September 2007
                : 109
                : 4
                : 217-221
                Affiliations
                aMedical Intensive Care Unit, INSERM U 651, and Departments of bCardiology, cNephrology, and dPublic Health, Université Paris XII, Centre Hospitalier Universitaire Henri Mondor, Assistance Publique – Hôpitaux de Paris, Créteil, France
                Article
                107783 Cardiology 2008;109:217–221
                10.1159/000107783
                17873484
                © 2007 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: 3, References: 27, Pages: 5
                Categories
                Original Research

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