Heart disease is the leading cause of adult death in the United States. Chronic ischemia resulting from obstruction of coronary arteries is a major contributor to onset and progression of heart disease. Hibernating myocardium is a clinical condition in which chronic ischemia results in viable, yet persistently dysfunctional, myocardium. On a molecular level, the mitochondrial proteome is depressed, contributing to decreased energetic capacity. Hibernating myocardium is treated by coronary artery bypass graft surgery, restoring normal blood flow to the ischemic region of the heart. However, CABG results in variable and often incomplete recovery as evidenced by continued physiological and mitochondrial dysfunction. Oxidative stress and inflammation are believed to play primary roles in continued dysfunction. As such, we tested the hypothesis that inflammation is increased following CABG, resulting in increased oxidative stress and continued depression of mitochondrial proteins. In a swine model of revascularized hibernating myocardium, prostaglandin E2 was significantly increased in revascularized hibernating myocardium compared to healthy tissue. In a cell culture model, H9c2 cells treated with PGE2 exhibited increased production of markers of oxidative stress and decreased expression of mitochondrial electron transport chain proteins, supporting the potential role of inflammation in persistent dysfunction despite successful revascularization of hibernating myocardium.