Elevation of the glycoxidation product Nε-(carboxymethyl)lysine in patients presenting with acute myocardial infarction

Background: An important role in the acceleration of vascular disease has been previously suggested for advanced glycation end products. N e -(carboxymethyl)lysine (CML) is an advanced glycation end product formed on protein by combined non-enzymatic glycation and glycoxidation reactions. CML reacts with the receptor of advanced glycation end products inducing impairment of endothelium dependent relaxation and is a marker of oxidative stress. Methods: A total of 40 patients with acute myocardial infarction (17 patients with ST-elevation myocardial infarction, 23 patients with non-ST-elevation myocardial infarction) and 40 patients with stable coronary artery disease were included consecutively in this study. During coronary angiography, peripheral venous blood sample was taken for measuring CML. Results: Serum levels of CML were significantly increased in patients with acute myocardial infarction [17.9+10.7 vs. 6.6+3.1 arbitrary units (AU)/mg protein, p 9.5 AU/mg protein was associated with an odds ratio of acute myocardial infarction of 39.7 [95% confidence interval (CI): 11.1-142, p<0.001], a sensitivity of 0.85 (95% Cl: 0.70-0.94) and a specificity of 0.88 (95% Cl: 0.73-0.96). Conclusions: CML levels are significantly elevated in patients presenting with acute myocardial infarction. These results suggest the involvement of endothelial dysfunction (through receptor interaction) and oxidative stress in acute myocardial infarction.