Abstract
Despite several decades of advances in heart failure (HF) therapeutics resulting in substantial reductions in morbidity and mortality, symptomatic HF continues to be a major cause of mortality and hospitalization in the United States. Because of this, improved understanding of HF pathophysiology is crucial in developing novel and effective treatments for this syndrome. Oxidative stress is defined as an imbalance between the production and degradation of endogenously produced, highly reactive free radicals, also known as reactive oxygen species (ROS). Free radicals are atoms or molecules with an unpaired electron. In this regard, superoxide and nitric oxide represent primary examples of endogenously produced free radicals. One of the most convincing pieces of evidence that free radicals are implicated in the disruption of cardiac function is myocardial stunning—the phenomenon of prolonged cardiac dysfunction after brief periods of ischemia in the absence of irreversible injury. There is strong evidence suggesting that such stunning is associated with generation of ROS.