title: Plasma levels of high-sensitive C-reactive protein do not correlate with inflammatory activity in carotid atherosclerotic plaques.
abstract: BACKGROUND
  It is well established that subjects with moderately elevated plasma levels of C-reactive protein (CRP) have an increased risk of development of cardiovascular events. As atherosclerosis is a disease characterized by chronic arterial inflammation, it is possible that moderate increases in CRP level reflect the presence of plaque inflammation. To investigate this possibility, we compared plasma levels of hsCRP the day before carotid endarterectomy with the degree of inflammation in the excised plaque tissue.
  
  
  METHODS
  Luminex immunoassays were used to determine the levels of IL-6, IL-10, monocyte chemoattractant protein-1 and tumour necrosis factor-α (TNF-α) in plasma and in homogenized plaque tissue from 160 endarterectomy specimens. Plaque sections were stained with antibodies against CD68 to determine the plaque macrophage content.
  
  
  RESULTS
  Plasma high-sensitivity (hs)CRP levels were significantly correlated with plasma IL-6 and TNF-α. However, there were no significant associations between plasma hsCRP concentration and plaque cytokine levels or macrophage contents.
  
  
  CONCLUSIONS
  The present findings strongly argue against hsCRP as a marker of plaque inflammation. Hence, it is more likely that elevated hsCRP is a sign of a subclinical systemic inflammation and this in turn may contribute to progression of cardiovascular disease.
authors.affiliation: Experimental Cardiovascular Research Group, Clinical Research Center, Clinical Sciences, Lund University, Malmö, Sweden; Deptartment of Cardiology, Skåne University Hospital, Malmö, Sweden.
authors.forename: H
authors.initials: H
authors.lastname: Grufman
authors.forename: I
authors.initials: I
authors.lastname: Gonçalves
authors.forename: A
authors.initials: A
authors.lastname: Edsfeldt
authors.forename: M
authors.initials: M
authors.lastname: Nitulescu
authors.forename: A
authors.initials: A
authors.lastname: Persson
authors.forename: M
authors.initials: M
authors.lastname: Nilsson
authors.forename: J
authors.initials: J
authors.lastname: Nilsson
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism*; D016893:Carotid Stenosis / Q000097:blood* / Q000378:metabolism / Q000473:pathology; D018932:Chemokine CCL2 / Q000097:blood; D016207:Cytokines / Q000097:blood* / Q000378:metabolism; D005260:Female; D006801:Humans; D007118:Immunoassay; D007249:Inflammation / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000097:blood* / Q000378:metabolism / Q000473:pathology; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D016207:Cytokines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D002097:C-Reactive Protein
keywords: C-reactive protein; atherosclerotic plaque; cytokines; macrophage