Numerous studies have now shown that sustained elevation of aldosterone levels induces cardiovascular damage independent from its effects on regulation of renal sodium and blood pressure. Increased aldosterone and cortisol levels in patients with heart failure independently predict the risk of mortality. Over the past decade, there has been increased interest in identifying the role of the receptor for aldosterone, the mineralocorticoid receptor (MR), following the results from the large clinical heart failure trials that showed low doses of MR antagonists reduced morbidity and mortality in heart failure and myocardial infarction, even though plasma levels of aldosterone were in the physiologic range. The mechanism for this cardioprotective action remains to be defined, although changes in the redox state have been shown to play a key role in MR-mediated cardiac damage. This review will highlight some of these studies and provide an update on the action of aldosterone in heart disease.