Relationship between calculated total antioxidant status and atherosclerotic coronary artery disease
1Department of Surgical and Clinical Pathology, ehran Heart Center, Tehran University of Medical Sciences, Tehran- Iran
2Cardiac Research, Tehran Heart Center, Tehran University of Medical Sciences, Tehran- Iran
Anatol J Cardiol 2016; 9(16): 689-695 PubMed ID: 27488746 PMCID: 5331354 DOI: 10.5152/AnatolJCardiol.2015.6482
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Abstract

Objective: Antioxidants play a major role in the cellular protection cascade against oxidative damage. Oxidative stress has been linked to the pathogenesis of coronary atherosclerosis. Our aim was to evaluate the association between calculated serum total antioxidant status (cTAS) and the presence and severity of coronary artery disease (CAD).
Materials and Methods: One hundred and seventy-four patients with angiographically documented significant (≥50%) luminal stenosis (n=123) or with minimal (<50%) luminal stenosis (n=51) in at least one coronary artery or major branch segment in the epicardial coronary tree were categorized as CAD+ group; 88 patients with no luminal stenosis were considered as the control group. The level of cTAS (mmol/L) was evaluated using the following equation: (0.63×albumin concentration)+(1.02×uric acid concentration)+(1.53×bilirubin concentration).
Results: In univariate analyses, mean levels of cTAS, uric acid, and creatinine were significantly higher in CAD+ group than in controls. However, adjusted cTAS level was not found to be a CAD predictor in the total population [odds ratio (OR)=1.20; 95% confidence interval (CI): 0.81–1.76;p=0.364] or in men (OR=1.25; 95% CI: 0.73–2.12; p=0.420) and women (OR=1.20; 95% CI: 0.66–2.19; p=0.553). A weak but statistically significant correlation was found between cTAS and Gensini score (Spearman’s ρ=0.16, p=0.015).
Conclusion: In patients with suspicious CAD, the level of cTAS was not found to be an independent predictor for the presence of CAD. Further studies with larger sample size are required to confirm the results. (Anatol J Cardiol 2016; 16: 689-95)