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Int J Angiol 2009; 18(4): 187-192
DOI: 10.1055/s-0031-1278352
Original Article

© Georg Thieme Verlag KG Stuttgart · New York

Low levels of soluble receptor for advanced glycation end products in non-ST elevation myocardial infarction patients

Erick D. McNair1 , Calvin R. Wells2 , A. Mabood Qureshi1 , Rashpal S. Basran2 , Colin Pearce2 , Jason Orvold2 , Jacobus Devilliers2 , Kailash Prasad3
  • 1Department of Pathology, College of Medicine, University of Saskatchewan, and Royal University Hospital, Saskatoon, Saskatchewan
  • 2Department of Cardiology, College of Medicine, University of Saskatchewan, and Royal University Hospital, Saskatoon, Saskatchewan
  • 3Department of Physiology, College of Medicine, University of Saskatchewan, and Royal University Hospital, Saskatoon, Saskatchewan
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Publication History

Publication Date:
28 April 2011 (online)

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Abstract

BACKGROUND: Interaction of the receptors for advanced glycation end products (RAGEs) with advanced glycation end products (AGEs) results in expression of inflammatory mediators (tumor necrosis factor-alpha [TNF-α] and soluble vascular cell adhesion molecule-1 [sVCAM-1]), activation of nuclear factor-kappa B and induction of oxidative stress — all of which have been implicated in atherosclerosis. Soluble RAGE (sRAGE) acts as a decoy for the RAGE ligand and is protective against atherosclerosis.

OBJECTIVES: To determine whether levels of serum sRAGE are lower, and whether levels of serum AGEs, TNF-α and sVCAM-1 are higher in non-ST elevation myocardial infarction (NSTEMI) patients than in healthy control subjects; and whether sRAGE or the ratio of AGEs to sRAGE (AGEs/sRAGE) is a predictor/biomarker of NSTEMI.

METHODS: Serum levels of sRAGE, AGEs, TNF-α and sVCAM-1 were measured in 46 men with NSTEMI and 28 age- and sex-matched control subjects. Angiography was performed in the NSTEMI patients.

RESULTS: sRAGE levels were lower, and levels of AGEs, TNF-α, sVCAM-1 and AGEs/sRAGE were higher in NSTEMI patients than in control subjects. sRAGE levels were negatively correlated with the number of diseased coronary vessels, serum AGEs, AGEs/sRAGE, TNF-α and sVCAM-1. The sensitivity of the AGEs/sRAGE test is greater than that of the sRAGE test, while the specificity and predictive values of the sRAGE test are greater than those of the AGEs/sRAGE test for identifying NSTEMI patients.

CONCLUSIONS: Serum levels of sRAGE were low in NSTEMI patients, and were negatively correlated with extent of lesion, inflammatory mediators, AGEs and AGEs/sRAGE. Both sRAGE and AGEs/sRAGE may serve as biomarkers/predictors for identifying NSTEMI patients.