title: Angiogenesis, thrombogenesis, endothelial dysfunction and angiographic severity of coronary artery disease.
abstract: BACKGROUND
  Thrombogenesis, angiogenesis, and endothelial damage/dysfunction are components in the pathogenesis of atherosclerosis.
  
  
  OBJECTIVE
  To investigate the relation of these variables to atherosclerotic disease severity and the possible interrelations between the three.
  
  
  METHODS
  111 patients attending for coronary angiography were studied (85 male, 26 female; mean (SD) age, 61.6 (10.0) years). Plasma concentrations of von Willebrand factor (vWf, a marker of endothelial damage/dysfunction), vascular endothelial growth factor (VEGF, associated with angiogenesis), soluble VEGF receptor Flt-1 (sFlt-1), and tissue factor (TF, a key component of coagulation) were measured by an enzyme linked immunosorbent assay. Following angiography, disease severity was assessed by the number of coronary vessels diseased (> 50% stenosis) and by a coronary atheroma score.
  
  
  RESULTS
  All indices were raised in the patients compared with 34 healthy controls except sFlt-1, which was lower in the patients. No significant correlations were found between the coronary atheroma score and values of vWf (Spearman correlations: r = 0.21, p = 0.83), VEGF (r = 0.11, p = 0.27), or TF (r = -0.04, p = 0.68). However, there was an inverse correlation between plasma sFlt-1 and coronary atheroma score (r = -0.19, p = 0.049). The number of vessels diseased had no relation to any marker. Correlations were found between TF and VEGF (r = 0.25, p = 0.008) and between TF and sFlt-1 (r = 0.42, p < 0.001) in the patients.
  
  
  CONCLUSIONS
  Despite evidence of abnormal angiogenesis (VEGF and sFlt-1), thrombogenesis (TF), and endothelial damage/dysfunction (vWf) in the patients with coronary artery disease, there was no correlation between VEGF, sFlt-1, vWf, or TF and angiographically defined disease severity.
authors: Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK.
authors: N A
authors: NA
authors: Chung
authors: C
authors: C
authors: Lydakis
authors: F
authors: F
authors: Belgore
authors: F L
authors: FL
authors: Li-Saw-Hee
authors: A D
authors: AD
authors: Blann
authors: G Y H
authors: GY
authors: Lip
mesh_terms: D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000209:etiology* / Q000473:pathology; D003328:Coronary Thrombosis / Q000097:blood / Q000150:complications* / Q000473:pathology; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000097:blood / Q000150:complications / Q000473:pathology; D012044:Regression Analysis; D012307:Risk Factors; D013925:Thromboplastin / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D042461:Vascular Endothelial Growth Factor A; D014841:von Willebrand Factor; D013925:Thromboplastin; D040281:Vascular Endothelial Growth Factor Receptor-1