title: Coronary artery ectasia and inflammatory cytokines: link with a predominant Th-2 immune response?
abstract: OBJECTIVE
  The role of inflammation in coronary artery ectasia (CAE) remains controversial. We evaluated the hypothesis that CAE might be associated with a specific pattern of T helper (Th) lymphocyte activation by measuring the Th-1 cytokine, interleukin-2 (IL-2) and the Th-2 cytokines, interleukin-4 (IL-4) and interleukin-6 (IL-6) in patients with CAE, obstructive coronary artery disease (CAD) and controls.
  
  
  METHODS
  Serum levels of IL-2, IL-4 and IL-6 were measured in 74 patients undergoing an elective cardiac catheterization due to angina pectoris and positive or equivocal non-invasive screening for cardiac ischaemia: 34 had CAE and non-obstructive CAD (Group A), 22 had obstructive CAD (Group B) and 18 had normal coronaries (Group C).
  
  
  RESULTS
  Group A had significantly higher IL-4 than Group B and Group C (p<0.001 and p=0.006, respectively). In contrast, Group A had markedly lower IL-2 than Group B and Group C (p<0.001 for both comparisons). Group C had higher IL-4 and lower IL-2 than Group B (p<0.001 for both comparisons). Interleukin-6 was significantly higher in Groups A and B compared to Group C (p<0.001 for both comparisons), whilst it was comparable between Group A and Group B. Multivariate logistic regression analysis showed that higher levels of IL-4 and lower levels of IL-2 were the strongest independent predictors associated with CAE (OR: 3.846, CI: 1.677-8.822, p=0.001 and OR: 0.567, CI: 0.387-0.831, p=0.004, respectively).
  
  
  CONCLUSIONS
  Our data demonstrates that Th-2 immune response, exhibited through increased IL-4 and low IL-2, constitutes a fundamental feature of CAE.
authors.affiliation: Second Department of Cardiology, University of Athens Medical School, Attikon University Hospital, Athens, Greece.
authors.forename: Andreas S
authors.initials: AS
authors.lastname: Triantafyllis
authors.forename: Andreas S
authors.initials: AS
authors.lastname: Kalogeropoulos
authors.forename: Angelos G
authors.initials: AG
authors.lastname: Rigopoulos
authors.forename: Eleftherios A
authors.initials: EA
authors.lastname: Sakadakis
authors.forename: Ioannis K
authors.initials: IK
authors.lastname: Toumpoulis
authors.forename: Spyridon
authors.initials: S
authors.lastname: Tsikrikas
authors.forename: Dimitrios T
authors.initials: DT
authors.lastname: Kremastinos
authors.forename: Ioannis
authors.initials: I
authors.lastname: Rizos
mesh_terms: D003324:Coronary Artery Disease / Q000097:blood / Q000235:genetics / Q000276:immunology*; D003331:Coronary Vessels / Q000473:pathology; D004108:Dilatation, Pathologic / Q000097:blood / Q000235:genetics / Q000276:immunology*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000235:genetics / Q000276:immunology; D007376:Interleukin-2 / Q000097:blood*; D015847:Interleukin-4 / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D007376:Interleukin-2; D015850:Interleukin-6; D015847:Interleukin-4
keywords: Coronary artery disease; Coronary artery ectasia; Cytokines; Inflammation; T-helper lymphocytes