摘要
Background： Metabolic syndrome （MetS） is one of the high cardiovascular （CV） situations. Endothelial dysfunction, which is a common finding in patients with MetS, is related with increased CV risk. In patients with MetS, the effect of the major CV risk factors, not included in the MetS definition, on endothelial dysfunction is not well known. The aim of this study was to determine the effect of major CV risk factors such as gender, smoking, family history, and biochemical parameters on endothelial dysfunction in patients with MetS. Methods： The study was performed between December 2010 and August 2014. A total of 55 patients （ 15 females and 40 males） with MetS and 81 healthy controls （37 females and 44 males） with a body mass index 〈25 kg/m2 were enrolled in the study. Endothelial dysfunction was measured by flow-mediated dilatation （FMD）, oxidative stress parameters; high-sensitivity C-reactive protein （hs-CRP）, oxidized low-density lipoprotein （ox-LDL）, endothelial nitric oxide synthase （e-NOS）, nitric oxide, and cell adhesion markers; yon Willebrand factor, and e-selectin. Platelet aggregation （endothelial adenosine diphosphate）, total platelet count, and mean platelet volume were additionally analyzed and demographic parameters were explored. Student＇s t-test, Mann-Whitney U-test, and Chi-square test were used to analyze the results. Results： The fasting blood glucose （z = 3.52, P = 0.001 ）, hs-CRP （z - 3.23, P = 0.004）, ox-LDL （z = 2.62, P= 0,013）, and e-NOS （z = 2.22, P = 0.026） levels and cardiac risk score （z - 5.23, P 〈 0.001） were significantly higher in patients with MetS compared with the control group. Smoking was correlated with decreased FMD （χ2 = 9.26, P = 0.002） in MetS patients but not in the control group. Conclusions： Increased ox-LDL, hs-CRP, and e-NOS are likely to be a result of oxidative stress, a condition in which an imbalance occurs between the production and inactivation of reactive nitrogen and oxygen species. In addition, in patients with MetS, smoking is independently related to endothelial dysfunction.
Background： Metabolic syndrome （MetS） is one of the high cardiovascular （CV） situations. Endothelial dysfunction, which is a common finding in patients with MetS, is related with increased CV risk. In patients with MetS, the effect of the major CV risk factors, not included in the MetS definition, on endothelial dysfunction is not well known. The aim of this study was to determine the effect of major CV risk factors such as gender, smoking, family history, and biochemical parameters on endothelial dysfunction in patients with MetS. Methods： The study was performed between December 2010 and August 2014. A total of 55 patients （ 15 females and 40 males） with MetS and 81 healthy controls （37 females and 44 males） with a body mass index 〈25 kg/m2 were enrolled in the study. Endothelial dysfunction was measured by flow-mediated dilatation （FMD）, oxidative stress parameters; high-sensitivity C-reactive protein （hs-CRP）, oxidized low-density lipoprotein （ox-LDL）, endothelial nitric oxide synthase （e-NOS）, nitric oxide, and cell adhesion markers; yon Willebrand factor, and e-selectin. Platelet aggregation （endothelial adenosine diphosphate）, total platelet count, and mean platelet volume were additionally analyzed and demographic parameters were explored. Student＇s t-test, Mann-Whitney U-test, and Chi-square test were used to analyze the results. Results： The fasting blood glucose （z = 3.52, P = 0.001 ）, hs-CRP （z - 3.23, P = 0.004）, ox-LDL （z = 2.62, P= 0,013）, and e-NOS （z = 2.22, P = 0.026） levels and cardiac risk score （z - 5.23, P 〈 0.001） were significantly higher in patients with MetS compared with the control group. Smoking was correlated with decreased FMD （χ2 = 9.26, P = 0.002） in MetS patients but not in the control group. Conclusions： Increased ox-LDL, hs-CRP, and e-NOS are likely to be a result of oxidative stress, a condition in which an imbalance occurs between the production and inactivation of reactive nitrogen and oxygen species. In addition, in patients with MetS, smoking is independently related to endothelial dysfunction.
