In this study, we demonstrated that serum levels of NGAL are higher in patients with CAD than in healthy controls patients. Among ACS patients, these levels are gradually elevated according to the severity of the coronary clinical syndrome (UA, NSTEMI, and STEMI). Also serum levels of NGAL are higher in patients with ACS than in patients with SA and could be used, with high negative value, to discriminate patients with stable or unstable coronary syndromes. The relevance of NGAL to cardiovascular disease (CVD) remains primarily unknown. Elevated plasma NGAL levels were associated with atherosclerosis and were implicated as a predictor for cardiovascular mortality after cerebrovascular ischemia, possibly because of activation of blood leukocytes [18] [19] [20] . Although in recent reports has been shown that NGAL is present in atherosclerotic plaques and in human abdominal aortic aneurisms, raising the possibility that expression of NGAL can be induced in vascular cells during atherogenesis, the underlying mechanism for the induction of NGAL in vascular cells remains unknown [15, 21] . In further analysis the main source of NGAL was found to be neutrophils, probably recruited in the vascular wall by platelet activation [21] .