title: Hypercholesterolaemia impairs monocyte function in CAD patients.
abstract: OBJECTIVE
  Hypercholesterolaemia (HC) impairs arteriogenesis, i.e. collateral artery growth. Monocytes are crucial mediators of arteriogenesis. We investigated the impact of the cardiovascular risk factor HC on ligand-induced monocyte chemotaxis.
  
  
  METHODS
  The migratory response of monocytes towards the arteriogenic ligands vascular endothelial growth factor-A (VEGF-A) and monocyte chemoattractant protein-1 (MCP-1) in hypercholesterolaemic coronary artery disease (CAD) patients (n = 14), hypercholesterolaemic controls (n = 8) and age-matched healthy controls (n = 19) was analysed. Furthermore, the serum VEGF-A level was determined in all individuals.
  
  
  RESULTS
  VEGF-A-induced monocyte chemotaxis was severely impaired in hypercholesterolaemic CAD patients when compared with age-matched healthy controls (P < 0.001). The same was true for the migratory response towards MCP-1 (P < 0.001). VEGF-A- and MCP-1-induced monocyte chemotaxis of hypercholesterolaemic controls was also decreased in comparison with the healthy control group, but not as severe as observed in the hypercholesterolaemic CAD patients. VEGF-A serum levels did not differ between the three study groups.
  
  
  CONCLUSIONS
  Hypercholesterolaemia severely impairs monocyte function in hypercholesterolaemic CAD patients. Monocyte dysfunction is probably connected to impaired collateral artery growth. The duration of the cardiovascular risk factor HC seems to influence the extent of monocyte dysfunction, as there exists a continuum of diminished monocyte chemotaxis in the three study groups. Further trials are warranted in order to determine whether statins can reverse the negative influence of HC on cell function.
authors.affiliation: Department of Cardiology, University of Maastricht, Maastricht, the Netherlands.
authors.forename: F S
authors.initials: FS
authors.lastname: Czepluch
authors.forename: A
authors.initials: A
authors.lastname: Bergler
authors.forename: J
authors.initials: J
authors.lastname: Waltenberger
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000494:pharmacology; D002633:Chemotaxis; D008078:Cholesterol, LDL / Q000097:blood; D003097:Collateral Circulation; D003324:Coronary Artery Disease / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000502:physiology*; D019821:Simvastatin / Q000627:therapeutic use; D018709:Statistics, Nonparametric; D042461:Vascular Endothelial Growth Factor A / Q000494:pharmacology
chemical_list: D000924:Anticholesteremic Agents; D018932:Chemokine CCL2; D008078:Cholesterol, LDL; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D019821:Simvastatin