Serum Levels of Vascular Endothelial Growth Factor in Patients with Acute Myocardial Infarction Undergoing Reperfusion Therapy

1997 ◽  
Vol 92 (5) ◽  
pp. 453-454 ◽  
Author(s):  
Yoshinori Seko ◽  
Yasushi Imai ◽  
Shin Suzuki ◽  
Shuichi Kamijukkoku ◽  
Kazuya Hayasaki ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Serum Levels ◽  
Reperfusion Therapy ◽  
Vascular Endothelial ◽  
Early Reperfusion ◽  
Healthy Control ◽  
Endothelial Growth Factor

1. Vascular endothelial growth factor, a potent angiogenic mitogen, is known to be induced in response to ischaemia as well as being secreted from tumour cells. However, the precise mechanism of vascular endothelial growth factor release in acute myocardial infarction and the effects of coronary reperfusion on the circulating levels of vascular endothelial growth factor are still unknown. 2. Nineteen patients with acute myocardial infarction who underwent early reperfusion therapy were studied. Serum levels of vascular endothelial growth factor before reperfusion were markedly increased as compared with those in 19 healthy control subjects [252.4 ± 158.1 pg/ml (mean ± SD) compared with undetectable]. After reperfusion, the serum vascular endothelial growth factor levels rapidly returned almost completely to the normal control range. 4. These data strongly suggest that the serum level of vascular endothelial growth factor is one of the most sensitive indicators of myocardial ischaemia.

Serum levels of endostatin, vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) in patients with acute myocardial infarction undergoing early reperfusion therapy

2004 ◽  
Vol 106 (5) ◽  
pp. 439-442 ◽  
Author(s):  
Yoshinori SEKO ◽  
Shuichi FUKUDA ◽  
Ryozo NAGAI
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Growth Factor ◽  
Serum Levels ◽  
Reperfusion Therapy ◽  
Vascular Endothelial ◽  
Early Reperfusion ◽  
Ischaemia Reperfusion ◽  
Endothelial Growth Factor ◽  
Hepatocyte Growth

Angiogenesis is controlled by anti-angiogenic factors as well as by angiogenic factors, such as VEGF (vascular endothelial growth factor) and HGF (hepatocyte growth factor). Endostatin, a potent endogenous angiogenesis inhibitor, is known to inhibit endothelial proliferation and suppress tumour growth. However, to date, little is known about the pathophysiology of endostatin in ischaemia/reperfusion. To investigate the mechanisms of angiogenesis induced by myocardial ischaemia/reperfusion in more detail, we studied the circulating levels of endostatin, VEGF and HGF in 17 patients with acute myocardial infarction, who underwent early reperfusion therapy. In all patients, serum endostatin, VEGF and HGF levels before reperfusion were increased significantly compared with those in 17 control subjects (endostatin, 49.2±11.7 ng/ml, but not detectable in controls; VEGF, 685.6±150.3 pg/ml compared with 173.7±33.6 pg/ml; HGF, 3638±1285 pg/ml compared with 59±13 pg/ml; values are means±S.E.M.). After reperfusion, the serum endostatin and VEGF levels decreased significantly, but still remained higher than those in control subjects (endostatin, 19.6±7.0 ng/ml; VEGF, 284.2±90.2 pg/ml). In contrast, serum HGF levels increased significantly (15 146±2230 pg/ml) after reperfusion. These data indicated that serum levels of endostatin changed in parallel with those of VEGF in response to myocardial ischaemia/reperfusion, and the marked increase in serum HGF levels after reperfusion seemed to be, at least in part, due to heparin administration. Our data offer a possible anti-endostatin therapy in patients with acute myocardial infarction to facilitate collateral vessel formation.

scholarly journals Cell Transplantation for the Treatment of Acute Myocardial Infarction Using Vascular Endothelial Growth Factor–Expressing Skeletal Myoblasts

Circulation ◽  
2001 ◽  
Vol 104 (suppl_1) ◽  
Author(s):  
Ken Suzuki ◽  
Bari Murtuza ◽  
Ryszard T. Smolenski ◽  
Ivan A. Sammut ◽  
Noriko Suzuki ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cardiac Function ◽  
Vascular Endothelial ◽  
Skeletal Myoblast ◽  
Skeletal Myoblasts ◽  
Endothelial Growth Factor ◽  
Host Myocardium

Background Vascular endothelial growth factor (VEGF) is a promising reagent for inducing myocardial angiogenesis. Skeletal myoblast transplantation has been shown to improve cardiac function in chronic heart failure models by regenerating muscle. We hypothesized that transplantation of VEGF-expressing myoblasts could effectively treat acute myocardial infarction by providing VEGF-induced cardioprotection through vasodilatation in the early phase, followed by angiogenesis effects in salvaging ischemic host myocardium combined with the functional benefits of newly formed, skeletal myoblast-derived muscle in the later phase. Methods and Results Primary rat skeletal myoblasts were transfected with the human VEGF 165 gene using hemagglutinating virus of Japan-liposome with >95% transfection efficiency. Four million of these myoblasts (VEGF group), control-transfected myoblasts (control group), or medium only (medium group) was injected into syngeneic rat hearts 1 hour after left coronary artery occlusion. Myocardial VEGF-expression increased for 2 weeks in the VEGF group, resulting in enhanced angiogenesis without the formation of tumors. Grafted myoblasts had differentiated into multinucleated myotubes within host myocardium. Infarct size (33.3±1.4%, 38.1±1.4%, and 43.7±1.6% for VEGF, control, and medium groups, respectively; P =0.0005) was significantly reduced with VEGF treatment, and cardiac function improved in the VEGF group (maximum dP/dt: 4072.0±93.6, 3772.5±101.1, and 3482.5±90.6 mm Hg/s in the 3 groups, respectively; P =0.0011; minimum dP/dt: −504.2±68.5, −2311.3±57.0, and −2124.0±57.9 mm Hg/s, respectively; P =0.0008). Conclusions This combined strategy of cell transplantation with gene therapy could be of importance for the treatment of acute myocardial infarction.

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