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Far from being a direct complication of primary damage to heart muscle, it is now recognised that the pathogenesis of heart failure may rely on a combination of neurohormonal, cellular and molecular factors. An overwhelming number of systems appear to be activated in heart failure and contribute in some way towards structural remodelling. Comprising a comprehensive evaluation of the experimental and clinical data relating oxidative stress and heart failure, this text proposes that oxidative stress may be the common pathway for muscle dysfunction, cellular growth and remodelling, and mytocyte death. Acknowledged experts in the field here present a persuasive argument for raising the profile of oxidative stress as an important, perhaps critical contributor to the adverse consequences of heart failure. This volume should serve as a rich source of supportive data for clinicians and investigators interested in the pathophysiology and treatment of heart failure, and as a platform on which to base further research.