title: Multiple inflammatory markers in patients with significant coronary artery disease.
abstract: BACKGROUND
  Several inflammatory biomarkers are linked to cardiovascular risk. In order to investigate their coexistence and relative responses, several established and two novel markers (lactoferrin and the terminal complement complex), representing infection and central components of inflammation, were measured simultaneously in patients undergoing first-time coronary angiography.
  
  
  RESULTS
  Blood samples from patients with (n=131) or without (n=103) significant coronary artery stenosis were analyzed for plasma markers representing endothelium, platelets, neutrophils, monocytes, and complement, C-reactive protein, and antibodies against the infectious agents Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus. In multivariate logistic regression analysis, hypercholesterolemia (p<0.001), increased concentrations of the neutrophil activation marker lactoferrin (p<0.001) and the monocyte activation marker neopterin (p=0.012), lower concentrations of the terminal complement complex (p<0.001), and antibodies against C. pneumoniae (p=0.023) were variables linked to coronary artery stenosis. In univariate analysis additional relationships were found to current smoking (p<0.001), increased plasma concentrations of vascular cell adhesion molecule-1 (p=0.015), E-selectin (p<0.01), myeloperoxidase (p=0.051) and endothelin-1 (p=0.053), as well as diabetes (p=0.039).
  
  
  CONCLUSIONS
  Activation of multiple inflammatory pathways and C. pneumoniae infection may influence the inflammatory response in atherosclerosis. These pilot data provide an indication of the relative usefulness of various inflammatory biomarkers, indicating that the novel markers lactoferrin and the terminal complement complex warrant further investigation.
authors.affiliation: Department of Laboratory Medicine, Children's and Women's Health, The Norwegian University of Science and Technology, Norway. Vibeke.Videm@ntnu.no
authors.forename: Vibeke
authors.initials: V
authors.lastname: Videm
authors.forename: Rune
authors.initials: R
authors.lastname: Wiseth
authors.forename: Sigurd
authors.initials: S
authors.lastname: Gunnes
authors.forename: Hans O
authors.initials: HO
authors.lastname: Madsen
authors.forename: Peter
authors.initials: P
authors.lastname: Garred
mesh_terms: D000704:Analysis of Variance; D002097:C-Reactive Protein / Q000378:metabolism; D016009:Chi-Square Distribution; D015938:Complement Membrane Attack Complex / Q000378:metabolism; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood* / Q000000981:diagnostic imaging; D019040:E-Selectin / Q000097:blood; D019332:Endothelin-1 / Q000097:blood; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007781:Lactoferrin / Q000097:blood; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D019798:Neopterin / Q000097:blood; D009195:Peroxidase / Q000097:blood; D012307:Risk Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015938:Complement Membrane Attack Complex; D019040:E-Selectin; D019332:Endothelin-1; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D019798:Neopterin; D002097:C-Reactive Protein; D009195:Peroxidase; D007781:Lactoferrin