Plasma neutrophil gelatinase-associated lipocalin levels in acute myocardial infarction and stable coronary artery disease

Abstract

Introduction: 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). Conclusion: 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. © 2011 Wolters Kluwer Health. Lippincott Williams & Wilkins.