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      Increased Blood Vascular Endothelial Growth Factor Levels in Patients with Acute Myocardial Infarction

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          Abstract

          Vascular endothelial growth factor (VEGF) is a growth factor for vascular endothelial cells in vitro. The present study was designed to determine whether serum VEGF levels increase in patients with acute myocardial infarction (AMI) compared with patients with stable exertional angina and control subjects, and to examine the serial changes of serum VEGF levels in patients with AMI. We examined serum VEGF levels by using antibody prepared from serum immunized with human VEGF<sub>121</sub>. The serum VEGF level (pg/ml) was higher (p < 0.0001) on admission in the patients with AMI (177 ± 19) than in those with stable exertional angina (61 ± 7) and control subjects (62 ± 6). The serum VEGF level (pg/ml) of the patients with AMI was 177 ± 19 on admission, 125 ± 9 on day 3, 137 ± 11 on day 5, 242 ± 18 at 1 week, and 258 ± 22 at 2 weeks after admission. The value was higher on admission than on day 3 after admission (p = 0.014), the values were higher at 1 week and 2 weeks than on admission, on day 3, and 5 (p < 0.01). Furthermore, there were correlations between peak VEGF levels at 1 week or 2 weeks after admission and peak creatine kinase levels. The increase of VEGF on admission in the patients with AMI may be due to the hypoxia of acute myocardial ischemia. The elevation at 1 week and 2 weeks from the onset may cause the development of collateral circulation in relation to the healing of the infarction site.

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          Most cited references 5

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          Vascular endothelial growth factor is a potential tumour angiogenesis factor in human gliomas in vivo.

           G Breier,  H Weich,  W Risau (1992)
          Clinical and experimental studies suggest that angiogenesis is a prerequisite for solid tumour growth. Several growth factors with mitogenic or chemotactic activity for endothelial cells in vitro have been described, but it is not known whether these mediate tumour vascularization in vivo. Glioblastoma, the most common and most malignant brain tumour in humans, is distinguished from astrocytoma by the presence of necroses and vascular proliferations. Here we show that expression of an endothelial cell-specific mitogen, vascular endothelial growth factor (VEGF), is induced in astrocytoma cells but is dramatically upregulated in two apparently different subsets of glioblastoma cells. The high-affinity tyrosine kinase receptor for VEGF, flt, although not expressed in normal brain endothelium, is upregulated in tumour endothelial cells in vivo. These observations strongly support the concept that tumour angiogenesis is regulated by paracrine mechanisms and identify VEGF as a potential tumour angiogenesis factor in vivo.
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            Constitutive production and thrombin-induced release of vascular endothelial growth factor by human megakaryocytes and platelets

             R Mohle,  R Nachman,  M Moore (1997)
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              Hypoxia is a strong inducer of vascular endothelial growth factor mRNA expression in the heart.

               C Frelin,  A Ladoux (1993)
              Vascular endothelial growth factor (VEGF) is a potent and specific mitogen for vascular endothelial cells. A 3.9 kb VEGF transcript is expressed by all cardiac tissues from rat, mouse and guinea pig examined. VEGF expression was not developmentally regulated. The major form of VEGF mRNAs expressed by cardiac tissues coded for VEGF188. Myocyte enriched and fibroblast enriched cultures of new born rat heart cells also expressed VEGF transcripts but the major mRNA found coded for VEGF164. The expression of VEGF mRNA in myocyte enriched cultures of new born rat ventricles was increased 2 fold by serum, 5 fold by phorbol myristate acetate and 7 fold by hypoxic conditions. We conclude that hypoxic conditions may promote cardiac capillary cell growth by inducing VEGF expression.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2000
                June 2000
                04 July 2000
                : 93
                : 1-2
                : 93-99
                Affiliations
                aDepartment of Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto and bBioscience Research Department, Toagosei Co. Ltd., Tsukuba Research Laboratory, Tsukuba, Ibaraki, Japan
                Article
                7008 Cardiology 2000;93:93–99
                10.1159/000007008
                10894913
                © 2000 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: 29, Pages: 7
                Categories
                Coronary Care

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