title: Matrix metalloproteinases and inflammatory markers in coronary artery ectasia: their relationship to severity of coronary artery ectasia.
abstract: OBJECTIVE
  Although underlying mechanisms of coronary artery ectasia (CAE) are clearly unknown, destruction of extracellular matrix may be responsible for the ectasia formation. Thus, we investigated the role of matrix metalloproteinases (MMP), tissue inhibitor of matrix metalloproteinases (TIMP-1), and inflammatory markers [high-sensitive C-reactive protein, interleukins (ILs)] in CAE patients.
  
  
  METHODS
  This study consisted of 28 consecutive CAE patients, 27 obstructive coronary artery disease (CAD) patients, and 22 controls with normal coronary arteries undergoing cardiac catheterization. Plasma levels of MMP-3, MMP-9, TIMP-1, and inflammatory markers were measured.
  
  
  RESULTS
  Plasma level of MMP-3 was significantly higher in CAE patients compared with both CAD patients and controls (17.2+/-6.1, 11.2+/-3.2, and 9.2+/-3.4 ng/ml, respectively, both P=0.001) and so did MMP-9 level (27.4+/-5.9, 24.8+/-4.4, and 20.6+/-4.6 ng/ml, respectively, both P<0.05). IL-6 level was also higher in CAE patients than in controls (60.9+/-22.1 vs. 36.1+/-21.5 pg/ml, P=0.001) but were comparable in CAE and CAD patients. Plasma high-sensitive C-reactive protein, IL-1, and TIMP-1 levels were similar in three groups. MMP-3 levels correlated with diffuse (r=0.46, P=0.01) and multivessel ectasia (r=0.45, P=0.02).
  
  
  CONCLUSIONS
  Our results suggest that the increased level of MMP-3, MMP-9, and IL-6 may be responsible for ectasia formation in patients with CAE.
authors.affiliation: Department of Cardiology, School of Medicine, Suleyman Demirel University, Isparta, Turkey. adogan35@hotmail.com
authors.forename: Abdullah
authors.initials: A
authors.lastname: Dogan
authors.forename: Nurullah
authors.initials: N
authors.lastname: Tuzun
authors.forename: Yasin
authors.initials: Y
authors.lastname: Turker
authors.forename: Selahattin
authors.initials: S
authors.lastname: Akcay
authors.forename: Selcuk
authors.initials: S
authors.lastname: Kaya
authors.forename: Mehmet
authors.initials: M
authors.lastname: Ozaydin
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D003323:Coronary Aneurysm / Q000000981:diagnostic imaging / Q000201:enzymology / Q000276:immunology; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000201:enzymology / Q000276:immunology; D004108:Dilatation, Pathologic; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D007375:Interleukin-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D019278:Matrix Metalloproteinase 3 / Q000097:blood*; D020780:Matrix Metalloproteinase 9 / Q000097:blood*; D020782:Matrix Metalloproteinases / Q000097:blood*; D008875:Middle Aged; D011446:Prospective Studies; D012720:Severity of Illness Index; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000097:blood
chemical_list: D015415:Biomarkers; C508600:IL6 protein, human; D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D019715:Tissue Inhibitor of Metalloproteinase-1; D002097:C-Reactive Protein; D020782:Matrix Metalloproteinases; C511768:MMP3 protein, human; D019278:Matrix Metalloproteinase 3; D020780:Matrix Metalloproteinase 9