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      Long-Term Changes in Collagen Formation Expressed by Serum Carboxyterminal Propeptide of Type-I Procollagen and Relation to Left Ventricular Function after Acute Myocardial Infarction

      a , b , a

      Cardiology

      S. Karger AG

      Collagen remodeling, Myocardial infarction, Prognosis

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          Abstract

          The purpose of this study was to investigate the long-term sequential changes in serum levels of the carboxyterminal propeptide of type-I procollagen (s-PICP), which is a marker of type-I collagen synthesis, and to assess its clinical value in relation to left ventricular (LV) function and prognosis following acute myocardial infarction (AMI). Forty-eight consecutive patients with their first AMI and 15 control subjects were studied. Patients with AMI were stratified according to the changes in s-PICP levels between days 1 and 90 (ΔPICP) and divided into group I with ≤16.0 µg/l or group II with >16.0 µg/l. Patients in group II were characterized by LV dilatation, no improvement in ejection fraction and development of impaired diastolic filling from day 1 to 360, findings which were in contrast to group I. Cox regression analysis identified changes in s-PICP of >16.0 µg/l as an independent predictor of cardiac death or heart failure during follow-up. In conclusion, ΔPICP relates to long-term changes in LV function and size, and provides prognostic information following AMI.

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          Circulating Levels of Carboxyterminal Propeptide of Type I Procollagen and Left Ventricular Remodeling after Myocardial Infarction

          Alteration in myocardial collagen metabolism is an important factor in the progression of ventricular remodeling after myocardial infarction (MI). This study examined sequential changes in circulating levels of carboxyterminal propeptide of type I procollagen (PICP) as a collagen synthesis marker in order to assess the value of PICP for predicting the progression of left ventricular remodeling after MI. The study group comprised 20 patients with first MI undergoing reperfusion therapy. Peripheral blood samples were obtained on admission and serially up to 4 weeks after admission. Circulating levels of PICP and B-type natriuretic peptide (BNP), a tentative biochemical marker for the severity of MI, were measured by direct radioimmunoassay. Left ventricular end-diastolic volume index (EDVI) in acute and chronic phases were determined by left ventriculography, and changes (Δ) in EDVI were used as an index of left ventricular remodeling. Plasma PICP levels in the non-dilation group ( median ΔEDVI) PICP started to increase significantly 3 days after admission, peaking on day 14 (from 74 ± 6 to 104 ± 19 ng/ml, p < 0.05). ΔEDVI was significantly correlated with plasma PICP at 2 and 3 weeks, and with plasma BNP at 1, 2 and 3 weeks. Plasma PICP 2 weeks after MI was the only independent predictor of ΔEDVI (p < 0.001). These results suggest that an increase in plasma PICP levels 2 weeks after admission is a useful biochemical predictor of the progression of ventricular remodeling after MI.
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            Author and article information

            Journal
            CRD
            Cardiology
            10.1159/issn.0008-6312
            Cardiology
            S. Karger AG
            0008-6312
            1421-9751
            2001
            November 2001
            08 November 2001
            : 96
            : 1
            : 45-50
            Affiliations
            aDepartment of Medicine, Section of Cardiology, Haderslev Hospital, Haderslev, and bLaboratory of Rheumatology, Hvidovre Hospital, Copenhagen, Denmark
            Article
            47385 Cardiology 2001;96:45–50
            10.1159/000047385
            11701940
            © 2001 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, Tables: 2, References: 26, Pages: 6
            Categories
            Coronary Care

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