title: Antiendothelial cell antibodies in patients with coronary artery ectasia.
abstract: BACKGROUND
  The mechanisms involved in the pathogenesis of coronary artery ectasia (CAE) have not been elucidated. Circulating antiendothelial cell antibodies (AECA) are often detectable in systemic vasculitis and have been implicated in the pathogenesis of endothelial injury. Their prevalence in CAE is not known.
  
  
  RESULTS
  Out of 475 consecutive patients subjected to coronary angiography, 27 patients were diagnosed with CAE. Thirty patients matched for age, body mass index, sex, and coronary artery disease prevalence, served as controls. Serum AECA of IgG, IgM, and IgA isotypes were detected using a cell-based enzyme-linked immunosorbent assay (ELISA). Antinuclear antibodies (ANA) and antineutrophil cytoplasmic antibodies (ANCA) were detected using indirect immunofluorescence. IgG and IgM anticardiolipin antibodies (aCL) were detected using commercial ELISA. The prevalence of ANA and ANCA was similar in CAE patients and controls (33.3 vs. 43.3%, and 3.3 vs. 7.4%, respectively). There was no significant difference in IgG or IgM aCL reactivity between patients and controls. Both CAE patients and controls were negative for IgG AECA. The frequency of IgM AECA positivity was similar in CAE patients and controls. The prevalence of AECA of the IgA isotype was significantly higher in CAE patients (37.0 vs. 10%, P<0.05).
  
  
  CONCLUSIONS
  There is increased prevalence of circulating AECA of the IgA isotype in patients with CAE. This provides evidence for a role of autoimmunity in the pathogenesis of certain cases of CAE.
authors.affiliation: Department of Cardiology, Athens Euroclinic, Athens, Greece. dkatritsis@euroclinic.gr
authors.forename: Demosthenes G
authors.initials: DG
authors.lastname: Katritsis
authors.forename: Theodoros
authors.initials: T
authors.lastname: Zografos
authors.forename: Socrates
authors.initials: S
authors.lastname: Korovesis
authors.forename: Eleftherios
authors.initials: E
authors.lastname: Giazitzoglou
authors.forename: Pierre
authors.initials: P
authors.lastname: Youinou
authors.forename: Fotini N
authors.initials: FN
authors.lastname: Skopouli
authors.forename: Haralampos M
authors.initials: HM
authors.lastname: Moutsopoulos
mesh_terms: D000368:Aged; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000097:blood; D000974:Antibodies, Antinuclear / Q000097:blood; D001323:Autoantibodies / Q000097:blood*; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000276:immunology*; D003331:Coronary Vessels / Q000276:immunology* / Q000473:pathology; D004108:Dilatation, Pathologic; D042783:Endothelial Cells / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D006115:Greece; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D008297:Male; D008875:Middle Aged; D015854:Up-Regulation
chemical_list: D019268:Antibodies, Antineutrophil Cytoplasmic; D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M