title: Vascular endothelial growth factor serum concentrations in hypercholesterolemic patients.
abstract: OBJECTIVE
  Vascular endothelial growth factor (VEGF) promotes normal and pathological angiogenesis. VEGF is a chemotactic factor for macrophages and vascular smooth muscle cells, and induces synthesis of metalloproteinases and adhesion molecules. VEGF expression is regulated by hypoxia, cytokines, oncogenes, and oxidized low-density lipoprotein (LDL). The purpose of this study was to determine the relationship between levels of lipid parameters and VEGF, to investigate whether pravastatin treatment influences VEGF serum concentrations, and to examine the relationship between VEGF and the variations in post-treatment lipid and inflammatory parameters.
  
  
  METHODS
  Eighteen patients aged 48+/-6.8 years with total cholesterol (TC) >6.1 mmol/L comprised the hypercholesterolemic group. The controls included 12 individuals aged 50+/-7.4 years with TC <5.1 mmol/L. TC, high-density lipoprotein cholesterol (HDLC), triglycerides, LDLC, C-reactive protein (CRP), and VEGF were determined in both groups at baseline, and in the hypercholesterolemic group after 4 months of treatment with 20 mg/day pravastatin.
  
  
  RESULTS
  A significant correlation was observed between concentrations of VEGF and TC, LDLC and TG, and a significant difference in VEGF concentration was observed between the control group (mean 142 ng/L) and the hypercholesterolemic group (mean 272.9 ng/L). A significant decrease was observed in TC (14.7 %), LDLC (21.5 %), CRP (22.7 %), and VEGF (14.8 %) after 4 months of treatment with pravastatin.
  
  
  CONCLUSIONS
  A relationship was found between serum levels of VEGF and most atherogenic lipoproteins. In patients with hypercholesterolemia treated with pravastatin, a reduction in VEGF and CRP was seen in addition to lipid decreases.
authors.affiliation: Department of Laboratory Medicine, Hospital de Sant Joan de Déu, Althaia Xarxa Assistencial de Manresa, Barcelona, Spain. jtrape@yahoo.es
authors.forename: J
authors.initials: J
authors.lastname: Trapé
authors.forename: C
authors.initials: C
authors.lastname: Morales
authors.forename: R
authors.initials: R
authors.lastname: Molina
authors.forename: X
authors.initials: X
authors.lastname: Filella
authors.forename: J M
authors.initials: JM
authors.lastname: Marcos
authors.forename: R
authors.initials: R
authors.lastname: Salinas
authors.forename: J
authors.initials: J
authors.lastname: Franquesa
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic; D017035:Pravastatin / Q000627:therapeutic use; D014280:Triglycerides / Q000097:blood; D042461:Vascular Endothelial Growth Factor A / Q000097:blood*
chemical_list: D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D018836:Inflammation Mediators; D014280:Triglycerides; D042461:Vascular Endothelial Growth Factor A; D002097:C-Reactive Protein; D002784:Cholesterol; D017035:Pravastatin