ORIGINAL ARTICLE Advanced glycation end products in myocardial reperfusion injury Peter Celec • Ju ´lius Hodosy • Peter Ja ´ni • Pavol Janega • Matu ´s ˇ Ku ´ dela • Marta Kalousova ´ • Johana Holzerova ´ • Vojtech Parra ´k • Luka ´c ˇ Halc ˇa ´k • Toma ´s ˇ Zima • Martin Braun • Ivan Pecha ´n ˇ • Ja ´n Murı ´n • Katarı ´na S ˇ ebekova ´ Received: 4 August 2010 / Accepted: 8 April 2011 / Published online: 12 May 2011 Ó Springer 2011 Abstract Advanced glycation end products (AGEs) are associated with cardiovascular diseases. Whether the AGE levels change during myocardial reperfusion injury is cur- rently unknown. The aim of our study was to investigate the dynamics of AGEs in myocardial reperfusion injury and to discuss potential reasons for these changes. The dynamics of AGEs, pentosidine and neopterin in the plasma of patients with acute myocardial infarction (AMI) treated using thrombolysis (n = 40) were analyzed. In addition, AGEs were measured in patients with open heart surgery (n = 12) and rabbits with induced AMI (n = 9). In all three studies of myocardial reperfusion injury, a significant decrease of AGEs was observed (by 26 ± 19% in patients with AMI, by 23 ± 14% in patients with open heart surgery and by 39 ± 10% in rabbits with AMI within 1 day of reperfusion; p \ 0.05 in all studies). In additional studies, an association between lower AGEs and an activated immune system (R 2 = 0.09; p \ 0.01) and fasting (decrease by 38%; p \ 0.01) was shown. AGEs decrease in reperfusion injury of the heart. Indices pointing towards the involvement of immune system activation and fasting are presented. Further Prof. Ivan Pecha ´n ˇ has deceased in Autumn 2010. P. Celec (&) Á J. Hodosy Á K. S ˇ ebekova ´ Institute of Molecular Biomedicine, Comenius University, Sasinkova 4, 811 08 Bratislava, Slovakia e-mail: petercelec@gmail.com P. Celec Á J. Holzerova ´ Institute of Pathophysiology, Comenius University, Bratislava, Slovakia P. Celec Department of Molecular Biology, Comenius University, Bratislava, Slovakia J. Hodosy Institute of Physiology, Comenius University, Bratislava, Slovakia J. Hodosy Á V. Parra ´k Á J. Murı ´n University Hospital, Comenius University, Bratislava, Slovakia P. Ja ´ni Department of Pathology, Hospital Krnov, Krnov, Czech Republic P. Janega Institute of Pathology, Comenius University, Bratislava, Slovakia P. Janega Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovakia M. Ku ´dela Department of Zoology, Comenius University, Bratislava, Slovakia M. Kalousova ´ Á T. Zima Institute of Clinical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, Prague, Czech Republic L. Halc ˇa ´k Institute of Chemistry, Biochemistry and Clinical Biochemistry, Comenius University, Bratislava, Slovakia M. Braun Institute of Rheumatology, Prague, Czech Republic I. Pecha ´n ˇ National Institute of Cardiovascular Diseases, Bratislava, Slovakia 123 Heart Vessels (2012) 27:208–215 DOI 10.1007/s00380-011-0147-z