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

Clin Chem Lab Med. 2009;47(4):446-51. doi: 10.1515/CCLM.2009.100.


Background: An important role in the acceleration of vascular disease has been previously suggested for advanced glycation end products. N(epsilon)-(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<0.001]. A cut-off value of CML>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% CI: 0.70-0.94) and a specificity of 0.88 (95% CI: 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.

MeSH terms

  • Acute Disease
  • Aged
  • Female
  • Glycosides / metabolism*
  • Humans
  • Lysine / analogs & derivatives*
  • Lysine / blood
  • Male
  • Middle Aged
  • Myocardial Infarction / blood*
  • Oxidation-Reduction


  • Glycosides
  • N(6)-carboxymethyllysine
  • Lysine