In this review, we have examined the role of oxidative stress and apoptosis in the continuum of molecular changes that accompanies congestive heart failure. Cytokine activation and tumor necrosis factor-, in particular, may play a role in this continuum, favouring both oxidative stress and apoptosis. Carvedilol, a non selective - and -blocker, exerts an anti-apoptotic effect on both the myocytes and the endothelial cells as a consequence of its antioxidant activity. The ability of carvedilol to inhibit apoptosis may have important clinical relevance in congestive heart failure. It is also important to emphasise that, in congestive heart failure, apoptosis occurs, not only in the heart, but also in the periphery. An increased rate of endothelial apoptosis may explain the occurrence of endothelial dysfunction in congestive heart failure.