PMID- 20231178
OWN - NLM
STAT- MEDLINE
DCOM- 20110311
LR  - 20151119
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 49
IP  - 6
DP  - 2010 Jun
TI  - Inflammatory markers in patients with coronary artery disease with and without 
      inflammatory rheumatic disease.
PG  - 1118-27
LID - 10.1093/rheumatology/keq005 [doi]
AB  - OBJECTIVES: Patients with inflammatory rheumatic diseases (IRDs) have a higher 
      morbidity and mortality from accelerated atherosclerosis than the general 
      population. We hypothesized that patients with the combination of IRD and 
      coronary artery disease (CAD) would have a certain inflammatory phenotype 
      compared with CAD patients without this comorbidity. METHODS: Four groups of 
      patients were included: patients with IRD, referred to coronary artery bypass 
      grafting (CABG) (CAD-IRD, n = 67), patients without IRD, referred to CABG (CAD, n 
      = 52), patients with IRD without CAD (IRD, n = 32) and healthy controls (n = 30). 
      Plasma levels of several inflammatory markers were analysed by enzyme 
      immunoassays. RESULTS: (i) Plasma levels of markers of endothelial cell 
      activation [i.e. vascular cell adhesion molecule-1 (VCAM-1) and von Willebrand 
      factor] and osteoprotegerin (OPG) were significantly increased and plasma levels 
      of CCL21 significantly decreased in CAD-IRD patients as compared with CAD 
      patients without IRD. (ii) Within the CAD-IRD group, acute coronary syndrome was 
      a significant predictor of OPG, suggesting an enhanced inflammatory response 
      during plaque destabilization in CAD-IRD patients. (iii) Plasma levels of VCAM-1, 
      OPG and CCL21, but not lipid parameters, IRD characteristics and several other 
      inflammatory markers (e.g. CRP), were significant predictors of CAD-IRD as 
      opposed to CAD in two logistic regression models. CONCLUSION: Our findings 
      further support a role for inflammation in the accelerated form of 
      atherosclerosis in IRD patients, and suggest that certain inflammatory pathways, 
      such as the enhanced endothelial cell activation and the RANK ligand/RANK/OPG 
      system, may be of particular importance.
FAU - Breland, Unni M
AU  - Breland UM
AD  - Research Institute of Internal Medicine, Rikshospitalet University Hospital, 
      Oslo, Norway.
FAU - Hollan, Ivana
AU  - Hollan I
FAU - Saatvedt, Kjell
AU  - Saatvedt K
FAU - Almdahl, Sven M
AU  - Almdahl SM
FAU - Damas, Jan K
AU  - Damas JK
FAU - Yndestad, Arne
AU  - Yndestad A
FAU - Mikkelsen, Knut
AU  - Mikkelsen K
FAU - Forre, Oystein T
AU  - Forre OT
FAU - Aukrust, Pal
AU  - Aukrust P
FAU - Ueland, Thor
AU  - Ueland T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100315
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
RN  - 0 (Biomarkers)
RN  - 0 (Chemokines)
RN  - 0 (Osteoprotegerin)
SB  - IM
MH  - Aged
MH  - Biomarkers/*metabolism
MH  - Case-Control Studies
MH  - Chemokines/*metabolism
MH  - Coronary Artery Disease/*complications/metabolism
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Models, Biological
MH  - Osteoprotegerin/*metabolism
MH  - Regression Analysis
MH  - Rheumatic Diseases/*complications/metabolism
MH  - Risk Factors
EDAT- 2010/03/17 06:00
MHDA- 2011/03/12 06:00
CRDT- 2010/03/17 06:00
PHST- 2010/03/17 06:00 [entrez]
PHST- 2010/03/17 06:00 [pubmed]
PHST- 2011/03/12 06:00 [medline]
AID - keq005 [pii]
AID - 10.1093/rheumatology/keq005 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2010 Jun;49(6):1118-27. doi: 10.1093/rheumatology/keq005. 
      Epub 2010 Mar 15.