title: Hepatocyte growth factor and vascular endothelial growth factor in ischaemic heart disease.
abstract: BACKGROUND
  Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are endothelial cell-specific growth factors, but the production of these growth factors in cardiomyocytes has also been demonstrated. However, there have been no reports focusing their attention on the changes in these growth factors after coronary intervention. We investigated the time-course changes of the serum VEGF and HGF levels in angina pectoris (AP) and acute myocardial infarction (AMI).
  
  
  METHODS
  The serum HGF and VEGF levels were measured in 60 patients with AP, in 62 patients with AMI (AP, before heparin administration, and at 24 and 48 hours, and one week after intervention; AMI, before heparin, and at 48 and 72 hours, and one, two, three and four weeks) and in 56 patients with neurocirculatory asthenia as controls. We defined the patients with remodelling who showed an increase in left ventricular end-diastolic volume index (LVEDVI) in the sub-acute phase of AMI.
  
  
  RESULTS
  Hepatocyte growth factor levels in the AP and AMI were significantly higher than that in the control (p<0.0001). The AMI level was also significantly higher than AP (p<0.001). In the AMI and AP, HGF peaked at 48 hours. Vascular endothelial growth factor level in the AMI was significantly higher than that in the control and AP (p<0.0001). In the AMI, VEGF peaked at two weeks. There was a significant positive correlation between the peak VEGF and LVEDVI in the sub-acute phase of AMI (p=0.0089, r=0.436). Peak VEGF in the remodelling (+) group was significantly higher than that in the remodelling (-) group (p<0.001). In the AP, VEGF was unchanged.
  
  
  CONCLUSIONS
  While both myocardial and vascular damage contribute to an increase in HGF level, vascular damage is not associated with the increase in VEGF. Vascular endothelial growth factor might be related to left ventricular remodelling in the sub-acute phase of myocardial infarction.
authors.affiliation: The Third Department of Internal Medicine, Showa University, School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan. hrsuzuki@med.showa-u.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Suzuki
authors.forename: Mikitaka
authors.initials: M
authors.lastname: Murakami
authors.forename: Makoto
authors.initials: M
authors.lastname: Shoji
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Iso
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kondo
authors.forename: Masayuki
authors.initials: M
authors.lastname: Shibata
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ezumi
authors.forename: Yuji
authors.initials: Y
authors.lastname: Hamazaki
authors.forename: Shinji
authors.initials: S
authors.lastname: Koba
authors.forename: Takashi
authors.initials: T
authors.lastname: Katagiri
mesh_terms: D000704:Analysis of Variance; D000787:Angina Pectoris / Q000097:blood*; D016022:Case-Control Studies; D005260:Female; D006493:Heparin / Q000008:administration & dosage; D017228:Hepatocyte Growth Factor / Q000097:blood*; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D013997:Time Factors; D042442:Vascular Endothelial Growth Factors / Q000097:blood*
chemical_list: D042442:Vascular Endothelial Growth Factors; D017228:Hepatocyte Growth Factor; D006493:Heparin