Angiotensin-converting enzyme (ACE) inhibitor therapy only partially suppresses aldosterone production and ‘aldosterone escape’ occurs in up to 40% of patients with congestive heart failure (CHF). The RALES and EPHESUS studies show clearly that even in the presence of ACE inhibitor therapy, aldosterone contributes to mortality in CHF. There are many mechanisms for this. Firstly, aldosterone contributes to endothelial dysfunction and attenuates endothelium-dependent vasodilatation, at least partly by reducing nitric oxide bioavailability. Aldosterone also promotes myocardial fibrosis and cardiac remodelling by enhancing collagen synthesis, resulting in increased myocardial stiffness and increased left ventricular mass. These mechanisms mediated by aldosterone contribute to increased risk of ventricular arrhythmias and sudden cardiac death. Inhibition of aldosterone’s effect on mineralocorticoid receptors should now be considered standard therapy in populations of CHF patients. Aldosterone blockers also reduce the blood pressure in all types of hypertensive patients and may have an additional role as add-on therapy in hypertension, especially to lessen target organ damage.