Clin Res Cardiol 96: Suppl 1 (2007)

P513 - Elevation of the glycoxidation product N -carboxymethyllysine (CML) in patients presenting with acute coronary syndromes (ACS)
S. Kralev1, E. Rautits1, S. Lang1, D. Haghi1, H.-P. Hammes2, T. Süselbeck1
1I. Medizinische Klinik, Universitätsklinikum Mannheim, Mannheim; 2V. Medizinische Klinik, Universitätsklinikum Mannheim, Mannheim;
Background: An important role in the acceleration of vascular disease has been previously suggested for advanced glycation end products (AGE). N-Carboxymethyllysine (CML) is an AGE formed on protein by combined nonenzymatic glycation and oxidation (glycoxidation) reactions. Serum concentrations of CML reflect integrated oxidative stress over long periods of time. Whether intracellular oxidative stress is associated with the risk of ACS has not been investigated.
Methods: Within one year (2005) 70 patients (40 pat. with ACS and 30 pat. with stable coronary artery disease (CAD) as control group) were included in this study. The control group of patients with CAD was matched to the ACS patient group (17 patients with STEMI, 23 patients with NSTEMI) according to age (+/- 1 year) and gender. All patients underwent coronary angiography. During the investigation a peripheral venous blood sample was taken for measuring serum level of CML.
Results: In the ACS group serum levels of CML (17.9±10.7 vs. 6.7±2.9, p=0.0001) were significantly increased. The ROC curve for CML measurements confirmed CML as a predictor of ACS (area under curve [AUC]: 0.87; 95% CI: 0.78-0.96; P<0.001). Cut-off value CML > 9.5 derived from the ROC analysis was associated with a 4.8 (2.3-9.9) Relative Risc of ACS (95% CI), P value < 0.0001, Sensitivity (95% CI) 0.85 (0.70-0.94) and Specificity (95% CI) 0.87 (0.69-0.96).
Conclusions: This is the first study showing that the serum level of CML - a major advanced glycation end product in vivo - is significantly elevated in patients presenting with ACS. We emphasize the importance of oxidative stress conditions in patients with ACS, suggesting that additionally to the release of inflammatory markers oxidative stress contributes to acute plaque rupture.