Progression of Coronary Artery Disease (CAD) from Stable Angina (SA) Towards Myocardial Infarction (MI): Role of Oxidative Stress 40-43
Dr. Neha Uppal,
68, Basant Avenue, Opposite, Basant Park, Amritsar, Punjab-143001, India.
Phone: 09501009212, E-mail: email@example.com
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.