title: Markers of inflammation and rapid coronary artery disease progression in patients with stable angina pectoris.
abstract: BACKGROUND
  Both endothelial cell activation and macrophage activation play a significant role in atherogenesis and atheromatous plaque vulnerability and may determine rapid coronary artery disease (CAD) progression. We sought to assess the association between serum inflammatory markers and rapid CAD progression in patients with chronic stable angina pectoris.
  
  
  RESULTS
  We studied 124 chronic stable angina pectoris patients (84 men; mean age, 61+/-10 years) who were on a waiting list for coronary angioplasty for a mean time of 4.8+/-2.4 months. CAD progression was defined as > or =10% diameter reduction of a pre-existing stenosis > or =50%, > or =30% diameter reduction of a stenosis <50%, development of a new stenosis > or =30% in a previously normal segment, or progression of any stenosis to total occlusion. CAD progression occurred in 35 patients (28%). After adjustment with binary logistic regression, neopterin (P<0.001), high-sensitivity C-reactive protein (P=0.017), matrix metalloproteinase-9 (P=0.002), soluble intercellular adhesion molecule 1 (P<0.001), and previous history of unstable angina (P=0.01) were independent predictors of rapid CAD progression. The association between rapid disease progression and inflammatory markers remained significant even when presence of complex lesions was introduced into the multivariate model.
  
  
  CONCLUSIONS
  Rapid CAD progression in patients with stable angina pectoris is associated with increased C-reactive protein levels and raised concentrations of biochemical markers of endothelial and macrophage activation.
authors.affiliation: Coronary Artery Disease Research Unit, Department of Cardiological Sciences, St George's Hospital Medical School, London, UK.
authors.forename: Emmanouil
authors.initials: E
authors.lastname: Zouridakis
authors.forename: Pablo
authors.initials: P
authors.lastname: Avanzas
authors.forename: Ramón
authors.initials: R
authors.lastname: Arroyo-Espliguero
authors.forename: Salim
authors.initials: S
authors.lastname: Fredericks
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Kaski
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood*; D015415:Biomarkers; D002097:C-Reactive Protein / Q000032:analysis*; D015897:Comorbidity; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood*; D023903:Coronary Restenosis / Q000097:blood; D023921:Coronary Stenosis / Q000097:blood / Q000000981:diagnostic imaging; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000378:metabolism; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008262:Macrophage Activation; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000097:blood; D020780:Matrix Metalloproteinase 9 / Q000097:blood*; D008875:Middle Aged; D019798:Neopterin / Q000032:analysis; D012307:Risk Factors; D012995:Solubility; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015415:Biomarkers; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D019798:Neopterin; D002097:C-Reactive Protein; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9