MITOCHONDRIAL ANTIOXIDANT MITOQUINONE MITIGATES CONTRACTILE DYSFUNCTION AND OXIDATIVE STRESS IN EARLY PHASE OF ACUTE MYOCARDIAL INFARCTION

Myocardial infarction (MI) is considered the primary cause of heart failure. Oxidative stress in the adjacent non-infarcted myocardium is believed to play a crucial role in the progression of left ventricular remodeling in the weeks following acute MI. At 7 days post-MI, the decrease in myocardial contractility is associated with alterations in Ca2+ handling and reactive oxygen species (ROS). Nevertheless, the impact of mitochondrial ROS as a source on contractile dysfunction during the early phase of MI remains unknown. Our hypothesis is that treatment with the mitochondrial antioxidant MitoQ for 7 days following MI will improve contractile function dependent on reduction on mitochondrial ROS production in the acute phase of MI.