title: Plasma neutrophil gelatinase-associated lipocalin levels in acute myocardial infarction and stable coronary artery disease.
abstract: BACKGROUND
  Inflammation and polymorphonuclear neutrophils are shown to be important in the pathogenesis of acute myocardial infarction (AMI). Neutrophil gelatinase-associated lipocalin (NGAL) is secreted from neutrophils and may increase the proteolytic activity within the atherosclerotic plaque. We aimed to investigate whether the plasma levels of NGAL are higher in patients with AMI compared with stable coronary artery disease (CAD).
  
  
  METHODS
  The study population consisted of 128 eligible patients who underwent coronary angiography with the clinical diagnosis of CAD. Of the 128 patients included in the study, the diagnosis was ST-segment elevation myocardial infarction (STEMI) in 53 patients, non-ST-elevation myocardial infarction (NSTEMI) in 38 patients and stable CAD in 37 patients. Plasma level of NGAL was measured in all patients with an enzyme-linked immunosorbent assay method. We compared the plasma NGAL levels among the groups.
  
  
  RESULTS
  We found higher plasma NGAL levels in patients with AMI compared with the patients with stable CAD (146 ± 23 vs. 101 ± 53 ng/ml, P<0.001). The plasma NGAL levels between the subgroups of AMI were similar (145 ± 23.9 vs. 145 ± 23.4 ng/ml, P=not significant). In multivariate analysis, the independent factors related to AMI were current smoking (P=0.024), extent and severity of coronary atherosclerosis (P=0.030), and NGAL levels. The plasma NGAL level was independently related to the existence of AMI (odds ratio: 1.045, 95% confidence interval: 1.019-1.072, P=0.001). In patients with plasma NGAL level above 127 ng/ml, we observed a 12 times higher incidence of AMI (odds ratio: 12.2, 95% confidence interval: 2.3-64, P=0.003).
  
  
  CONCLUSIONS
  The plasma level of NGAL is higher in patients with AMI compared with the patients with stable CAD. This finding may suggest an active pathophysiological role for NGAL in development of acute coronary events.
authors.affiliation: Department of Cardiology, School of Medicine, Gazi University, Ankara, Turkey. asifesah@yahoo.com
authors.forename: Asife
authors.initials: A
authors.lastname: Sahinarslan
authors.forename: Sinan Altan
authors.initials: SA
authors.lastname: Kocaman
authors.forename: Duygu
authors.initials: D
authors.lastname: Bas
authors.forename: Ahmet
authors.initials: A
authors.lastname: Akyel
authors.forename: Ugur
authors.initials: U
authors.lastname: Ercin
authors.forename: Ozlem
authors.initials: O
authors.lastname: Zengin
authors.forename: Timur
authors.initials: T
authors.lastname: Timurkaynak
mesh_terms: D000209:Acute-Phase Proteins; D000368:Aged; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood*; D004562:Electrocardiography; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D011518:Proto-Oncogene Proteins / Q000097:blood*
chemical_list: D000209:Acute-Phase Proteins; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins