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Current research is focused on the role of oxidative stress in the development of diabetic heart failure after myocardial infarction. Although it has been documented that an increased level of oxidative stress accompanies diabetes, little is know regarding oxidative stress associated with diabetic comorbid conditions such as myocardial infarction. It has been shown that after MI, diabetes is associated with greater myocardial oxidative stress burden and concomitant worsening of residual ventricular function.
In addition, a second group of studies has identified a specific "Type 1diabetic" pattern of cardiac proteome changes indicative of diabetic cardiomyopathy presenting with higher oxidative stress, which may independently and cooperatively contribute to impaired cardiac function and heart failure in the diabetic heart subsequent to myocardial infarction. Taken together, these studies suggest that analysis of isoprostane biosynthesis and protein expression profiles may be useful to predict the therapeutic response to established and novel antioxidant therapies for the prophylaxis of diabetic heart failure.
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