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首页> 外文期刊>Journal of Clinical and Diagnostic Research >Progression of Coronary Artery Disease (CAD) from Stable Angina (SA) Towards Myocardial Infarction (MI): Role of Oxidative Stress
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Progression of Coronary Artery Disease (CAD) from Stable Angina (SA) Towards Myocardial Infarction (MI): Role of Oxidative Stress

机译：稳定型心绞痛（SA）冠状动脉疾病（CAD）向心肌梗塞（MI）的发展：氧化应激的作用

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Introduction: There is now a consensus that atherosclerosis represents a state of heightened oxidative stress which is characterized by lipid and protein oxidation in the vascular wall. Inspite of many efforts which were made to explain the role of oxidative stress in progression of CAD (Coronary Artery Disease), its predictive role is still not clear. In order to fill these lacunae and to establish the utility of antioxidant vitamins in delaying the progression of CAD from stable angina (SA) towards myocardial Infarction (MI), the present study was conducted.Materials and Methods: In this study, we compared the lipid profile and oxidant antioxidant status in 50 patients of CAD and 50 controls. The 50 patients of CAD were further grouped into those with SA, unstable angina (USA) and MI and the values of blood reduced glutathione (GSH) and lipid peroxidation marker Malonyldialdehyde (MDA) were studied and compared in these three subgroups of CAD.Results: The values of MDA were significantly increased in patients of CAD as compared to those in controls. Plasma MDA values of patients who presented with unstable angina and acute MI were significantly higher than those in patients who presented with SA and in controls, whereas there was no significant difference between values in those with unstable angina and non Q wave MI. The values of GSH showed a significant depletion in patients of CAD as compared to those in controls. A clearly significant depletion in GSH levels was observed in SA patients as compared to those in unstable angina and MI. But no such variations were observed between unstable angina and MI patients.Conclusion: From the present study, it was concluded that there was a significant negative correlation between blood glutathione and serum MDA. This may have occurred due to utilization of GSH in quenching free radicals and still persisting oxidative stress, which may have caused an increase in MDA levels due to increased lipid peroxidation. Further, the enhanced depletion of GSH and the increase in the levels of MDA in patients of USA and MI as compared to those in SA patients confirms the role of oxidative stress in progression of CAD from SA through USA to MI.
机译：简介：现在已经达成共识，动脉粥样硬化代表着氧化应激加剧的状态，其特征是血管壁中的脂质和蛋白质氧化。尽管已经做出许多努力来解释氧化应激在CAD（冠状动脉疾病）进展中的作用，但是其预测作用仍然不清楚。为了填补这些缺陷并建立抗氧化剂维生素在延缓CAD从稳定型心绞痛（SA）向心肌梗塞（MI）进程中的作用，进行了本研究。材料与方法：在本研究中，我们比较了50名CAD患者和50名对照的血脂谱和氧化剂抗氧化剂状态。将这50例CAD患者进一步分为SA，不稳定型心绞痛（USA）和MI患者，并在这三个CAD组中比较了血液还原型谷胱甘肽（GSH）和脂质过氧化标记物丙二醛（MDA）的值并进行了比较。 ：与对照组相比，CAD患者的MDA值显着增加。不稳定型心绞痛和急性心肌梗死患者的血浆MDA值显着高于SA和对照组的血浆MDA值，而不稳定型心绞痛和非Q波心肌梗死的患者的血浆MDA值无显着差异。与对照组相比，CAD患者的GSH值显着减少。与不稳定型心绞痛和心梗患者相比，SA患者的GSH水平明显减少。但在不稳定型心绞痛和心肌梗死患者之间未观察到这种变化。结论：从本研究中可以得出结论，血液谷胱甘肽与血清MDA之间存在显着的负相关。这可能是由于在淬灭自由基中利用GSH并仍然持续存在氧化应激而发生的，这可能是由于脂质过氧化作用增加而导致MDA含量增加。此外，与SA患者相比，美国和MI患者中GSH的耗竭增加和MDA水平的增加证实了氧化应激在CAD从SA通过美国到MI的进展中的作用。

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