title: Markers of eosinophilic inflammation and risk prediction in patients with coronary artery disease.
abstract: BACKGROUND
  The eotaxin family comprises three distinct peptides (eotaxin, eotaxin-2 and eotaxin-3) which have been implicated in eosinophilic inflammation. In vitro and clinical studies suggest that eotaxins could play a role in vascular inflammation, but no data are available on their prognostic significance in patients with angiographically documented coronary artery disease (CAD).
  
  
  METHODS
  Baseline plasma samples were obtained from 1014 patients with documented CAD. We tested the predictive effect of markers of eosinophilic inflammation and C-reactive protein (CRP) on death from cardiovascular causes and nonfatal myocardial infarction over a 2.7-4.1-year follow-up period.
  
  
  RESULTS
  Unexpectedly, lower eotaxin-3 concentrations were observed in patients with adverse cardiovascular events, whereas both eotaxin and eotaxin-2 showed no association with risk. After adjustment for most potential confounders, patients in the upper-quartile of eotaxin-3 levels had a 0.42 hazard-ratio (95% CI, 0.29-0.61, P < 0.001) for adverse events compared with subjects in the lower-quartile. The highest risk of future cardiovascular events was observed in subjects with combined elevation of CRP and reduction of eotaxin-3; 4.4 hazard-ratio (95% CI, 2.1-9.5, P < 0.001). Importantly, receiver-operating-characteristic curves analysis suggested a superior prognostic value of eotaxin-3 compared with CRP for predicting cardiac events in patients with CAD.
  
  
  CONCLUSIONS
  Low levels of eotaxin-3 are an independent predictor of future adverse cardiovascular events in patients with CAD and may be useful for risk stratification.
authors.affiliation: Department of Hematological, Pneumological and Cardiovascular Sciences, University of Pavia, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Falcone
authors.forename: P
authors.initials: P
authors.lastname: Minoretti
authors.forename: A
authors.initials: A
authors.lastname: D'Angelo
authors.forename: M P
authors.initials: MP
authors.lastname: Buzzi
authors.forename: E
authors.initials: E
authors.lastname: Coen
authors.forename: E
authors.initials: E
authors.lastname: Emanuele
authors.forename: A
authors.initials: A
authors.lastname: Aldeghi
authors.forename: V
authors.initials: V
authors.lastname: Olivieri
authors.forename: D
authors.initials: D
authors.lastname: Geroldi
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D000075906:Chemokine CCL26; D019742:Chemokines, CC / Q000097:blood*; D015986:Confounding Factors, Epidemiologic; D003327:Coronary Disease / Q000097:blood* / Q000276:immunology / Q000401:mortality; D004802:Eosinophilia / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000276:immunology / Q000401:mortality; D011379:Prognosis; D016016:Proportional Hazards Models; D012372:ROC Curve; D018570:Risk Assessment
chemical_list: D015415:Biomarkers; C515456:CCL11 protein, human; C515484:CCL24 protein, human; C120429:CCL26 protein, human; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D000075906:Chemokine CCL26; D019742:Chemokines, CC; D002097:C-Reactive Protein