title: Serum levels of YKL-40 increases in patients with acute myocardial infarction.
abstract: OBJECTIVE
  YKL-40 is secreted by macrophages, including those in atherosclerotic plaques, neutrophils, and vascular smooth muscle cells. Circulating YKL-40 is elevated in patients with inflammation and increased tissue remodeling. The aim was to examine the sequential changes in serum YKL-40 in patients with acute myocardial infarction (AMI), with and without thrombolytic therapy, as compared with patients with stable coronary artery disease (CAD).
  
  
  METHODS
  YKL-40 was measured by radioimmunoassay in serum from 63 patients. A total of 47 patients had their first AMI [30 with ST segment elevation myocardial infarction (STEMI) were thrombolyzed, 17 with non-STEMI were not thrombolyzed] and 16 patients had CAD.
  
  
  RESULTS
  Serum YKL-40 at the time of admission was higher in patients with AMI (median: 156 microg/l, range: 40-3000 microg/l) than in patients with CAD (median: 106 microg/l, range: 54-300 microg/l, P=0.048) and healthy participants (median: 102 microg/l, range: 38-514 microg/l, P<0.001). No difference in serum YKL-40 between CAD patients and healthy participants (P=0.89) was observed. No difference in serum YKL-40 between the AMI patients with or without ST-elevations (P=0.12) was observed. The maximum serum YKL-40 during the first 24 h after admission was higher in thrombolyzed STEMI patients than in the nonthrombolyzed, non-STEMI patients (P=0.01) and the CAD patients (P<0.0001). Serum YKL-40 declined consistently from the maximum value just after the AMI and during follow-up. Serum YKL-40 at 90, 180, and 360 days after AMI were significantly higher in nonthrombolyzed than in thrombolyzed patients (P=0.004, P=0.008, P=0.017, respectively).
  
  
  CONCLUSIONS
  These results demonstrated that serum concentrations of YKL-40 are greatly increased in AMI patients with and without thrombolytic therapy.
authors.affiliation: Department of Gastroenterology, Hvidovre Hospital, Denmark.
authors.forename: Camilla
authors.initials: C
authors.lastname: Nøjgaard
authors.forename: Nis B
authors.initials: NB
authors.lastname: Høst
authors.forename: Ib Jarle
authors.initials: IJ
authors.lastname: Christensen
authors.forename: Steen Hvitfeldt
authors.initials: SH
authors.lastname: Poulsen
authors.forename: Kenneth
authors.initials: K
authors.lastname: Egstrup
authors.forename: Paul A
authors.initials: PA
authors.lastname: Price
authors.forename: Julia S
authors.initials: JS
authors.lastname: Johansen
mesh_terms: D054392:Adipokines; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D000071451:Chitinase-3-Like Protein 1; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D037102:Lectins; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*
chemical_list: D054392:Adipokines; D015415:Biomarkers; C084533:CHI3L1 protein, human; D000071451:Chitinase-3-Like Protein 1; D005343:Fibrinolytic Agents; D006023:Glycoproteins; D037102:Lectins