title: Increased YKL-40 levels in patients with isolated coronary artery ectasia: an observational study.
abstract: OBJECTIVE
  YKL-40, a new biomarker of localized inflammation, is secreted by macrophages within the atherosclerotic plaques. Coronary artery ectasia (CAE) is a clinical entity with unclear etiopathogenesis. Some studies have revealed that CAE may be a form of atherosclerosis that has more localized and intense inflammatory properties than atherosclerosis. The goal of this study was to investigate YKL-40 and C-reactive protein (CRP) levels in patients with isolated CAE compared to patients with normal coronary arteries (NCA) and coronary artery disease (CAD).
  
  
  METHODS
  Our study has an observational and cross-sectional design. Forty-nine patients with isolated CAE (mean age: 60±10 years), 30 age-and gender-matched control participants with NCA (30 patients, mean age: 58±12 years) and 30 patients with CAD (mean age: 61±10 years), were included in the study. The relationship between YKL-40, CRP levels and the presence of CAE was investigated. Univariate and multiple logistic regression analysis were used for analysis of independent variables to predict CAE.
  
  
  RESULTS
  Serum YKL-40 levels were significantly different among study groups (NCA: 110±53 μg/L, CAE: 144±68 and CAD: 180±117, p=0.005). CAD group and CAE group had significantly higher YKL-40 levels than NCA group (p=0.004 and p=0.015, respectively). CRP was not significantly different between three groups. In addition, there were no any statistically significant differences, with respect to age, gender, the presence of hypertension or diabetes mellitus, and the smoking status (p>0.05). Logistic regression analysis revealed only YKL-40 level as the determinant of CAE (OR: 1.010, 95% CI: 1.001-1.019, p=0.027).
  
  
  CONCLUSIONS
  YKL-40 levels in patients with isolated CAE compared to patients with NCA were found significantly high and only YKL-40 level was established as the determinant of CAE. We believe that further studies are needed to clarify the possible causative roles of YKL-40 in patients with isolated CAE.
authors.affiliation: Departments of Cardiology, Faculty of Medicine, Rize University, Rize-Turkey. sinanaltan@gmail.com.
authors.forename: Turan
authors.initials: T
authors.lastname: Erdoğan
authors.forename: Sinan Altan
authors.initials: SA
authors.lastname: Kocaman
authors.forename: Mustafa
authors.initials: M
authors.lastname: Çetin
authors.forename: Murtaza Emre
authors.initials: ME
authors.lastname: Durakoğlugil
authors.forename: Aynur
authors.initials: A
authors.lastname: Kırbaş
authors.forename: Aytun
authors.initials: A
authors.lastname: Canga
authors.forename: Adnan
authors.initials: A
authors.lastname: Yılmaz
authors.forename: Sıtkı
authors.initials: S
authors.lastname: Doğan
authors.forename: Yüksel
authors.initials: Y
authors.lastname: Çiçek
mesh_terms: D054392:Adipokines / Q000097:blood*; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000378:metabolism*; D016022:Case-Control Studies; D000071451:Chitinase-3-Like Protein 1; D003324:Coronary Artery Disease / Q000097:blood*; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D037102:Lectins / Q000097:blood*; D008297:Male; D008875:Middle Aged
chemical_list: D054392:Adipokines; D015415:Biomarkers; C084533:CHI3L1 protein, human; D000071451:Chitinase-3-Like Protein 1; D037102:Lectins; D002097:C-Reactive Protein