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Int J Angiol 2011; 20(1): 049-054
DOI: 10.1055/s-0031-1272552
ORIGINAL ARTICLE

© Thieme Medical Publishers

Inverse Association between Cardiac Troponin-I and Soluble Receptor for Advanced Glycation End Products in Patients with Non-ST-Segment Elevation Myocardial Infarction

Erick D. McNair1 , Calvin R. Wells2 , A.M. Qureshi1 , Colin Pearce2 , Gudrun Caspar-Bell3 , Kailash Prasad4
  • 1Department of Pathology and Laboratory Medicine, College of Medicine, University of Saskatchewan and Royal University Hospital, Saskatoon, Saskatchewan, Canada
  • 2Department of Cardiology, College of Medicine, University of Saskatchewan and Royal University Hospital, Saskatoon, Saskatchewan, Canada
  • 3Department of Endocrinology, College of Medicine, University of Saskatchewan and Royal University Hospital, Saskatoon, Saskatchewan, Canada
  • 4Department of Physiology, College of Medicine, University of Saskatchewan and Royal University Hospital, Saskatoon, Saskatchewan, Canada
Further Information

Publication History

Publication Date:
14 March 2011 (online)

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ABSTRACT

Interaction of advanced glycation end products (AGEs) with the receptor for advanced AGEs (RAGE) results in activation of nuclear factor kappa-B, release of cytokines, expression of adhesion molecules, and induction of oxidative stress. Oxygen radicals are involved in plaque rupture contributing to thromboembolism, resulting in acute coronary syndrome (ACS). Thromboembolism and the direct effect of oxygen radicals on myocardial cells cause cardiac damage that results in the release of cardiac troponin-I (cTnI) and other biochemical markers. The soluble RAGE (sRAGE) compete with RAGE for binding with AGE, thus functioning as a decoy and exerting a cytoprotective effect. Low levels of serum sRAGE would allow unopposed serum AGE availability for binding with RAGE, resulting in the generation of oxygen radicals and proinflammatory molecules that have deleterious consequences and promote myocardial damage. sRAGE may stabilize atherosclerotic plaques. It is hypothesized that low levels of sRAGE are associated with high levels of serum cTnI in patients with ACS. The main objective of the study was to determine whether low levels of serum sRAGE are associated with high levels of serum cTnI in ACS patients. The serum levels of sRAGE and cTnI were measured in 36 patients with non-ST-segment elevation myocardial infarction (NSTEMI) and 30 control subjects. Serum levels of sRAGE were lower in NSTEMI patients (802.56 ± 39.32 pg/mL) as compared with control subjects (1311.43 ± 66.92 pg/mL). The levels of cTnI were higher in NSTEMI patients (2.18 ± 0.33 μg/mL) as compared with control subjects (0.012 ± 0.001 μg/mL). Serum sRAGE levels were negatively correlated with the levels of cTnI. In conclusion, the data suggest that low levels of serum sRAGE are associated with high serum levels of cTnI and that there is a negative correlation between sRAGE and cTnI.

KEYWORDS

Soluble receptor for advanced glycation end products - cardiac troponin-I - non-ST-elevation mycardial infarction - cytokines - oxidative stress - thromboembolism

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Kailash PrasadM.D. Ph.D. 

Department of Physiology, College of Medicine, University of Saskatchewan

107 Wiggins Road, Saskatoon, Saskatchewan, Canada S7N 5E5

Email: k.prasad@usask.ca

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