In two recent studies it was found that serum levels of NGAL were significantly elevated in patients with angiographically confirmed CAD compared to those with normal arteries or controls [24, 25] . Our data agree with these reports since we found that levels of serum-NGAL are significantly higher in patients with all clinical syndromes of CAD than in healthy controls, reinforcing the utility of NGAL as biomarker of detection and the extent of CAD. The expression of NGAL from vascular cells during atherogenesis can also explain the differences between patients with SA and control subjects with no risk factors observed in our study. In addition to its induction in the vessels after mechanistic injury, previous studies suggest that NGAL is strongly upregulated in atherosclerotic lesions and also in the heart after ischemic injury [15] . It is possible that NGAL produced by vascular cells could also be secreted into the systemic circulation.