PMID- 17241185
OWN - NLM
STAT- MEDLINE
DCOM- 20070220
LR  - 20131121
IS  - 0954-6820 (Print)
IS  - 0954-6820 (Linking)
VI  - 261
IP  - 2
DP  - 2007 Feb
TI  - Hypercholesterolaemia impairs monocyte function in CAD patients.
PG  - 201-4
AB  - OBJECTIVES: 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. SUBJECTS: 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.
FAU - Czepluch, F S
AU  - Czepluch FS
AD  - Department of Cardiology, University of Maastricht, Maastricht, the Netherlands.
FAU - Bergler, A
AU  - Bergler A
FAU - Waltenberger, J
AU  - Waltenberger J
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Intern Med
JT  - Journal of internal medicine
JID - 8904841
RN  - 0 (Anticholesteremic Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cholesterol, LDL)
RN  - 0 (VEGFA protein, human)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - AGG2FN16EV (Simvastatin)
SB  - IM
MH  - Aged
MH  - Anticholesteremic Agents/therapeutic use
MH  - Case-Control Studies
MH  - Chemokine CCL2/pharmacology
MH  - Chemotaxis
MH  - Cholesterol, LDL/blood
MH  - Collateral Circulation
MH  - Coronary Artery Disease/*blood/complications/physiopathology
MH  - Female
MH  - Humans
MH  - Hypercholesterolemia/*blood/complications/physiopathology
MH  - Male
MH  - Middle Aged
MH  - Monocytes/drug effects/*physiology
MH  - Simvastatin/therapeutic use
MH  - Statistics, Nonparametric
MH  - Vascular Endothelial Growth Factor A/pharmacology
EDAT- 2007/01/24 09:00
MHDA- 2007/02/21 09:00
CRDT- 2007/01/24 09:00
PHST- 2007/01/24 09:00 [pubmed]
PHST- 2007/02/21 09:00 [medline]
PHST- 2007/01/24 09:00 [entrez]
AID - JIM1753 [pii]
AID - 10.1111/j.1365-2796.2006.01753.x [doi]
PST - ppublish
SO  - J Intern Med. 2007 Feb;261(2):201-4. doi: 10.1111/j.1365-2796.2006.01753.x.