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In response to a variety of stressful conditions such as pressure overload, volume overload, myocardial infarction and different types of cardiomyopathies, the heart undergoes an adaptation process during which it grows in size, a phenomenon referred to as hypertrophy. During this compensatory phase, the heart is better able to meet the increased work demand. However, if left untreated for a prolonged period, it can advance into the decompensated hypertrophic or the failing stage. It is now clear that transition of heart hypertrophy to the failure stage involves a number of abnormalities which include ionic imbalances, impairment in energy production and utilization, altered calcium metabolism and defects in the contractile proteins. More recently, alterations in free radicals and “antioxidant reserve” have been identified in the hypertrophy as well as failing stages. Discussion in this review is focussed on the role of oxidative stress in both compensated and decompensated stages, in various animal models of heart failure. Some clinical data on oxidative stress in heart failure patients is also reviewed. It is suggested that an increase in oxidative stress may play a role in the pathogenesis of heart failure.