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

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          Abstract

          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) showed no significant change. However, in the 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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          Most cited references 2

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          Interstitial collagen is increased in the non-infarcted human myocardium after myocardial infarction.

          In this study we report the changes of interstitial collagen in the human non-infarcted interventricular septum after a myocardial infarction as well as in hypertrophic human hearts with or without hypertension. The collagen amount was determined with the Sirius Red morphometry technique, which enabled us to perform these studies on routinely processed, paraffin embedded sections. The collagen amount was significantly increased in the septum of infarct patients as compared to non-infarcted controls (P < 0.001). The collagen amount in the septum of the hypertensive hypertrophy group (HH) was significantly increased as compared to the non-hypertensive hypertrophy group (NHH) (P < 0.01). The collagen content in the NHH was not significantly different from the controls in the infarct group, while the collagen amount in the HH showed no significant difference to the collagen content in the infarct group. The results indicate that collagen deposition is increased in the non-infarcted myocardium after a myocardial infarction, as well as in the hypertensive hypertrophied myocardium. The data suggest that the appearance of excessive collagen is not mediated by cardiac hypertrophy per se, but that the underlying cause, infarction or hypertension, is the significant factor.
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            Monitoring fibrillar collagen turnover in hypertensive heart disease

             J. DÍEZ (1997)
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              Author and article information

              Journal
              CRD
              Cardiology
              10.1159/issn.0008-6312
              Cardiology
              S. Karger AG
              0008-6312
              1421-9751
              1999
              August 1999
              06 August 1999
              : 91
              : 2
              : 81-86
              Affiliations
              Second Department of Internal Medicine, Iwate Medical University, Iwate, Japan
              Article
              6884 Cardiology 1999;91:81–86
              10.1159/000006884
              10449877
              © 1999 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: 1, References: 31, Pages: 6
              Categories
              General Cardiology

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