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

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          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.

                Author and article information

                S. Karger AG
                June 2000
                04 July 2000
                : 93
                : 1-2
                : 93-99
                aDepartment of Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto and bBioscience Research Department, Toagosei Co. Ltd., Tsukuba Research Laboratory, Tsukuba, Ibaraki, Japan
                7008 Cardiology 2000;93:93–99
                © 2000 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 1, References: 29, Pages: 7
                Coronary Care


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