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BACKGROUND: Resistin and oxidative stress may play a role in the pathogenesis of coronary heart disease (CHD) including acute coronary syndrome (ACS). The aim of this study was to investigate the role of serum resistin and prooxidant-antioxidant balance (PAB) in ACS occurrence in order to differentiate it from stable angina. Moreover, we aimed to determine the correlation between resistin and PAB in patients with ACS and its difference from patients with stable CHD. METHODS: This cross-sectional, descriptive study was conducted on 50 patients with ACS and 50 patients with stable CHD who underwent coronary angiography (CAG). Serum resistin level was measured using enzyme-linked immunosorbent assay (ELISA). PAB and other variables were analyzed using standard methods. RESULTS: A significant increase in serum resistin and PAB was observed in patients with ACS (2.55 ± 0.13 ng/ml and 123.5 ± 5.58 HK unit, respectively) compared to patients with stable CHD (1.53 ± 0.12 ng/ml and 95.9 ± 2.7 HK unit, respectively) (P < 0.001). In addition, a significant positive correlation was seen between serum resistin and PAB in patients with ACS (r = 0.39; P = 0.005), but this correlation was not found in patients with stable CHD (r = 0.21; P = 0.140). Resistin (r = 0.52; P < 0.001) and PAB (r = 0.55; P < 0.001) were significantly associated with high-sensitivity C-reactive protein (hs-CRP) in patients with ACS, but this association was not found in patients with stable CHD (resistin: r = 0.24; P = 0.090; PAB: r = -0.02: P = 0.910). CONCLUSION: High serum resistin or PAB levels, and their association with the occurrence of ACS, can be used as a robust discriminating factor to differentiate ACS from stable CHD.
RESUMO
MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression. It seems that microRNA-21 (miR-21) and Visfatin, a novel adipocytokine, play roles in inflammation and atherosclerosis. The aim of this study was to investigate the association of miR-21 with Visfatin, inflammation, atherosclerosis and acute coronary syndrome (ACS). Based on coronary angiography and electrocardiogram (ECG), 53 patients with ACS and 52 patients with stable CAD were enrolled in this study. We assayed serum miR-21, Visfatin, and routine chemistries using quantitative reverse transcriptase polymerase chain reaction (QRT-PCR), enzyme-linked immunosorbent assay (ELISA) and automated analyzer, respectively. We used a regression analysis to describe the relationship between the variables. Serum miR-21 level in 2-ΔCt value was significantly higher in ACS patients (10.52 ± 1.01-fold) than the stable CAD patients (4.4 ± 0.79-fold) (F = 4.59, p < 0.001). In addition, serum Visfatin was significantly higher in ACS patients (17.5 ± 0.61 ng/ml) than the stable CAD patients (12.7 ± 0.49 ng/ml) (F = 2.62, p < 0.001). Furthermore, the serum miR-21 level correlated positively with serum Visfatin level (r = 0.26, p = 0.008), hs-CRP (r = 0.29, p = 0.003), age (r = 0.21, p = 0.034) and negatively with HDL-cholesterol (r = -0.28, p = 0.004). We concluded that the increased serum miR-21 and Visfatin may be involved in the pathogenesis of ACS through promoting inflammation or may result from inflammatory responses to ACS. Furthermore, the potential role of miR-21 and Visfatin in plaque instability and inflammation warrants further investigations.