Mineralocorticoid receptor (MR) activation has been shown to play a deleterious role in the development of heart disease in studies using specific MR antagonists (spironolactone, eplerenone) in experimental models and patients. Pharmacological MR blockade attenuates the transition to heart failure (HF) in models of systolic left ventricular dysfunction and myocardial infarction and of diastolic dysfunction, in rats and mice. In humans, MR antagonism is highly beneficial in patients with mild or advanced HF and post‐infarct HF. The consequences of aldosterone and MR activation for cardiac arrhythmia and its prevention/correction by MR antagonists are often underestimated. MR activation modulates cardiac electrical activity, causing atrial and ventricular arrhythmias. A pro‐arrhythmogenic effect of aldosterone (possibly partly dependent on fibrosis) has been suggested by several studies. Cardiac MR activation has important consequences for the control of cellular calcium homeostasis, action potential lengthening, the modulation of calcium transients and sarcoplasmic reticulum diastolic leaks, resulting in the promotion of rhythm disorders. Aldosterone/MR activation (in both cardiomyocytes and coronary vessels) results in vascular dysfunction, and also contributes to pro‐arrhythmogenic conditions. Taken together, these pro‐arrhythmic effects of aldosterone/MR may explain the highly beneficial effect of MR antagonism, decreasing the incidence of sudden death, observed in the RALES and EPHESUS studies. This article is protected by copyright. All rights reserved.