Recent views suggest that long-term exposure to elevated
aldosterone concentrations might result in cardiac, vascular, renal, and metabolic sequelae that occur independent of the blood pressure level. Indirect evidence of the untoward effects of
aldosterone on the heart has been clearly established in clinical studies that have tested the effects of
mineralocorticoid receptor antagonists in the treatment of
systolic heart failure. As it has become clear in recent years, the interaction between
aldosterone and the heart has to deal with additional actions of the
hormone on specific cell types, cellular mechanisms, and molecules that are involved in regulation of tissue responses, leading to
hypertrophy, remodeling, and
fibrosis. The majority of these effects are mediated by activation of the
mineralocorticoid receptors that are expressed in cardiomyocytes and cardiac fibroblasts, and mediate the genomic effects of the
hormone. Evidence of interactions between
aldosterone and the heart that occur independent of the renal effects of
aldosterone, however, is not limited to the context of
systolic heart failure and observations obtained in other disease states have led, together with findings of animal studies, to a better understanding of the potential benefits of
aldosterone antagonists. In this narrative overview, we highlight the most recent findings that have been obtained in experimental animal models and in clinical conditions that include, in addition to
systolic heart failure, primary
aldosteronism,
essential hypertension,
diastolic heart failure, and
arrhythmia.