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      Cardiac Troponin I and Creatine Kinase Isoenzyme MB in Patients with Intradialytic Hypotension

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          Abstract

          Background: Intradialytic hypotension (IH) has been long recognized as a common complication during hemodialysis (HD) therapy, but few studies have discussed IH-related myocardial injuries and the long-term prognosis of patients prone to IH (HP). Methods: We conducted a prospective study on 70 chronic HD patients who had no recent occurrences of acute coronary artery syndrome. The patients were divided into two groups: HP (n = 29) and IH resistant (n = 41). While they underwent HD therapy, we monitored and evaluated their baseline data and their patterns of cardiac troponin I (cTnI), creatine kinase, and creatine kinase isoenzyme MB. Results: The HP and IH-resistant patients had similar baseline cardiac marker levels that did not seem to be influenced by uneventful HD therapy. However, if during HD therapy the patients experienced an episode of symptomatic IH, they were found to have significant increases in the creatine kinase MB activity at the end of HD therapy and in the cTnI levels 44 h following HD. After 12 months, the HP patients with baseline cTnI levels ≧0.20 ng/ml were more likely to experience cardiovascular events or death (adjusted odds ratio 15.0, p = 0.012). Conclusions: Our study showed that, after symptomatic IH episodes, the HP patients were more likely to suffer occult myocardial injuries. HP patients who have high cTnI levels should be closely monitored for cardiovascular diseases.

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          Most cited references 12

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          Intracellular compartmentation of cardiac troponin T and its release kinetics in patients with reperfused and nonreperfused myocardial infarction.

          In a previous study on the diagnostic efficiency of troponin T measurements in patients with suspected acute myocardial infarction (AMI), the authors found a high variability of troponin T serum concentration changes on day 1 in patients with AMI who underwent thrombolytic treatment. Therefore, the aims of the present study were to investigate the intracellular compartmentation of troponin T and to analyze the effects of AMI reperfusion on the appearance kinetics of cardiac troponin T in serum. Cardiac troponin T was measured with a newly developed bideterminant sandwich assay using cardiospecific, affinity-purified polyclonal antibodies and peroxidase-labeled monoclonal antibody. An unbound cytosolic troponin T pool was found in ultracentrifuged homogenates of myocardial tissue of different species ranging from 0.013 to 0.036 mg/g wet weight. The soluble troponin T molecule had electrophoretic properties identical to troponin T compartmented in the myofibrils. The clinical study group comprised 57 patients with AMI undergoing thrombolytic treatment. Blood flow to the infarct zone and point of time of reperfusion were tested by immediate and late angiography. The appearance of troponin T in serum on day 1 after the onset of AMI depended strongly on reperfusion and on duration of ischemia before reperfusion. Thus, in patients with early reperfused AMI, a marked peak in troponin T serum concentrations was found at 14 hours after the onset of pain. This early troponin T peak was absent in patients with AMI reperfusion occurring greater than 5.5 hours after the onset of pain and in patients with nonreperfused AMI. By contrast, the kinetics of troponin T release after the first day after AMI were unaffected by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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            Laboratory diagnosis of patients with acute chest pain.

            The enzyme activities of creatine kinase (CK), its isoenzyme MB (CK-MB) and of lactate dehydrogenase isoenzyme 1 (LD-1) have been used for years in diagnosing patients with chest pain in order to differentiate patients with acute myocardial infarction (AMI) from non-AMI patients. These methods are easy to perform as automated analyses, but they are not specific for cardiac muscle damage. During the early 90's the situation changed. First creatine kinase MB mass (CK-MB mass) replaced the measurement of CK-MB activity. Subsequently cardiac-specific proteins troponin T (cTnT) and troponin I (cTnI) appeared on the scene, displacing LD-1 analysis. However, troponin concentrations in blood increase only from four to six hours after onset of chest pain. Therefore a rapid marker such as myoglobin, fatty acid binding protein or glycogen phosphorylase BB could be used in early diagnosis of AMI. On the other hand, CK-MB isoforms alone may also be useful in rapid diagnosis of cardiac muscle damage. Myoglobin, CK-MB mass, cTnT and cTnI are nowadays widely used in diagnosing patients with acute chest pain. Myoglobin is not cardiac-specific and therefore requires supplementation with some other analyses such as troponins to support the myoglobin value. Troponins are very highly cardiac-specific. Only the sera of some patients with severe renal failure, which requires hemodialysis, have elevated cTnT and/or cTnI without there being any evidence of cardiac damage. On the other hand, the latest studies have shown that elevated troponin levels in sera of hemodialysis patients point to an increased risk of future cardiac events in a similar manner to the elevated troponin values in sera of patients with unstable angina pectoris. In addition, the bedside tests for cTnT and cTnI alone or together with myoglobin and CK-MB mass can be used instead of quantitative analyses in the diagnosis of patients with chest pain. These rapid tests are easy to perform and they do not require expensive instrumentation. For routine clinical laboratory practice we suggest that in diagnosis of patients with chest pain, myoglobin and CK-MB mass measurements should be performed whenever they are requested (24 h/day) and cTnT or cTnI on admission to the hospital and then 4-6 and 12 hours later.
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              A comparison of troponin T and troponin I as predictors of cardiac events in patients undergoing chronic dialysis at a Veteran's Hospital: a pilot study.

              The purpose of this study was to prospectively evaluate the usefulness of the cardiac troponins as predictors of subsequent cardiac events in patients with chronic renal failure undergoing dialysis. Cardiac troponin T (cTnT) and I (cTnI) are cardiac markers that are specific for cardiac muscle. They are also excellent prognostic indicators for patients presenting with chest pain. Although cardiac disease is the leading cause of death in dialysis patients, standard methods to diagnose acute coronary syndromes in patients with renal failure are often misleading. A six-month prospective study was done in a university-affiliated Veterans Hospital's dialysis clinic. Forty-nine patients undergoing chronic dialysis with no complaints of chest pain were followed for cardiac events occurring in the six months after cardiac troponin measurements. These included unstable angina, acute myocardial infarction and cardiac death. An additional 83 patients with renal failure but who were not undergoing dialysis were also examined. Within six months all three dialysis patients with elevated cTnI at entry into the study suffered an adverse complication (specificity and positive predictive value = 100%). Twenty-five patients had cTnT elevated at >0.10 ng/ml (53%). Patients with diabetes were more likely to have elevated troponin T levels (64% vs. 25%, p = 0.01). All six patients developing cardiac events within three months had elevations of cTnT >0.1 ng/ml (sensitivity = 100%). Whereas the specificity of cTnT was only 56% for a near-term cardiac event, the negative predictive value of cTnT using a cutoff of 0.2 ng/ml, only nine of 49 dialysis patients (18%) had elevated levels. In patients with renal failure not undergoing dialysis, only three of 83 (4%) had elevated troponin I or T. None of these patients suffered a cardiac event in the next six months. This prospective pilot study clearly delineates the troponins as important prognosticators in asymptomatic otherwise "stable" patients on chronic dialysis, especially those with concomitant diabetes mellitus. It also appears that troponins are more likely to be elevated in dialysis patients than other patients with renal failure not on dialysis. The above suggests that the combination of cTnI and cTnT might be very effective in elucidating cardiac risks of patients with renal failure undergoing chronic dialysis.
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                Author and article information

                Journal
                BPU
                Blood Purif
                10.1159/issn.0253-5068
                Blood Purification
                S. Karger AG
                0253-5068
                1421-9735
                2004
                June 2004
                02 September 2004
                : 22
                : 4
                : 338-343
                Affiliations
                aDivision of Nephrology, bDivision of Cardiology, E-Da Hospital, I-Shou University and Shu-Zen College of Medicine and Management, Kaohsiung County, and cDivision of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
                Article
                79188 Blood Purif 2004;22:338–343
                10.1159/000079188
                15218282
                © 2004 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: 24, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/79188
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