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      Cardiac Troponin I Degradation in Serum of Patients with Hypertrophic Obstructive Cardiomyopathy Undergoing Percutaneous Septal Ablation

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          Abstract

          Introduction: Troponin has become the most important marker for diagnosing acute myocardial infarction, yet knowledge is scarce regarding appearance of specific degradation fragments in the blood. We have recently described the appearance of intact cardiac troponin I (cTnI) and 7 degradation products in patients suffering from ST-elevation myocardial infarction (STEMI) using Western blot analysis. However, the time resolution in STEMI patients is hampered by the rather vague time point ‘onset of pain’. We therefore sought to utilize a time-wise more reliable model of human myocardial necrosis: percutaneous transluminal septal myocardial ablation (PTSMA) of hypertrophic obstructive cardiomyopathy (HOCM). Here the iatrogenic induction of myocardial necrosis occurs in vivo, allowing us to investigate degradation of cTnI by the second. Methods: Blood samples were obtained from 8 patients with HOCM just prior to initiation of PTSMA and up to 50 h following the procedure. Western blot analysis was performed with subsequent analysis of relative intensities of the bands as compared to the degradation of cTnI in STEMI patients from the ASSENT-2 troponin substudy. Results: We demonstrate intact cTnI and 9 degradation products [molecular weight (MW) 12.0–23.5 kDa]. The bands were comparable in MW to degradation fragments in STEMI. Their early rise in intensity, occurring within few minutes after the alcohol injection, emphasizes how susceptible troponin bands are to chemical/ischemic insults. Moreover, two additional bands were visible in the PTSMA population. Conclusion: This work describes the degradation products of troponin I in HOCM patients undergoing PTSMA. The detected bands appear fast and are similar to degradations following STEMI. This model contributes to our knowledge of the degradation patterns of troponin in disease states, and may thus play a role in the interpretation of elevated troponin levels.

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          Most cited references 5

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          Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy.

           U Sigwart (1995)
          Surgery has been the only therapeutic option in patients with hypertrophic obstructive cardiomyopathy who are resistant to drug treatment and sequential pacemaker therapy. I describe a novel catheter-based technique that may replace surgical myocardial reduction in some patients. The technique aims at selective destruction of the hypertrophied part of the left side of the intraventricular septum. If temporary occlusion of the first major septal artery is shown to reduce the intraventricular pressure gradient significantly, absolute alcohol is injected through the inflated balloon catheter to produce a localised infarct. In the first three patients treated with this method, the size of the septal infarct was sufficient to eliminate any subaortic stenosis immediately. Clinical improvement has been maintained up to 12 months. Non-surgical reduction of the septum in hypertrophic obstructive cardiomyopathy warrants further clinical evaluation.
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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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              Percutaneous transluminal septal ablation in hypertrophic obstructive cardiomyopathy.

              Percutaneous transluminal septal myocardial ablation (PTSMA) by alcohol-induced occlusion of septal branches with resulting reduction of LV outflow-tract gradient (LVOTG) is a new treatment option in symptomatic patients with hypertrophic obstructive cardiomyopathy (HOCM). In 1996 and 1997 we treated 114 symptomatic patients (56 female; age 53.3 +/- 15.6 years; 5 patients with prior myectomy and 5 with DDD pacer; most in NYHA class III. Five patients underwent re-PTSMA after failed first treatment. In the first 30 patients 1 to 3 septal branches were occluded by injection of 3.4 +/- 1.6 ml absolute alcohol via the central lumen after balloon occlusion of the proximal part of the septal branch. In the remaining patients myocardial contrast echocardiography was available, so that only one branch needed to be occluded. LVOTG reduction was achieved in 107 (94%) patients: at rest from 73.8 +/- 36.5 to 18.6 +/- 19.7 mmHg (p < 0.00001). Maximal CK rise was 647 +/- 330 U/L. Two (1.8%) patients died during hospital stay. Due to permanent trifascicular block 11 (9.6%) patients required a permanent pacemaker. At 3 months follow-up in 87 patients we observed no cardiac complications, a further LVOTG reduction in 61 % patients, an ongoing symptomatic improvement (NYHA I or II; p < 0.0001 vs. pre PTSMA), and significant reduction of the left posterior wall thickness. PTSMA of HOCM results in significant reduction of LVOTG. Careful monitoring during hospital stay is necessary because of the potential risks of the induced therapeutic infarction. Mid-term follow-up showed ongoing symptomatic improvement without cardiac complications. Remodeling after circumscribed septal infarction results in further LVOTG reduction in over 50% of the patients.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2009
                September 2009
                02 July 2009
                : 114
                : 3
                : 167-173
                Affiliations
                aDivision of Cardiology, Aker University Hospital and Faculty of Medicine, bCenter for Heart Failure Research and cDepartment of Mathematics, University of Oslo, dHormone Laboratory, Aker University Hospital, and eInstitute for Experimental Medical Research, Ullevål University Hospital, Oslo, Norway; fThe Heart Center, Copenhagen University Hospital, Copenhagen, Denmark
                Article
                226596 Cardiology 2009;114:167–173
                10.1159/000226596
                19571537
                © 2009 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: 3, References: 11, Pages: 7
                Categories
                Original Research

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