“…While in vivo animal models of cardiac pathology have highlighted redox-balance as a mediator of heart failure progression the translation of this to a clinical setting is becoming more apparent. Congestive heart failure progression, dilated, and ischemic cardiomyopathy, end stage heart failure, chronic heart failure, and ethanol induced cardiac abnormalities are all associated with a concurrent rise in free radical generation (Jaatinen et al, 1993 ; Landmesser, 2002 ; Maack et al, 2003 ; Giordano, 2005 ; Kunishige et al, 2007 ; Nakamura et al, 2015 ; Shah, 2015 ). Additionally, it is emerging that the enzymes and cellular sources driving increased ROS production may be divergent depending on the pathology involved such as systolic vs. diastolic dysfunction (Münzel et al, 2015 ).…”