The cardiac mineralocorticoid receptor (MR) has been clearly implicated in the development of various pathologies including heart hypertrophy, inflammation, fibrosis, apoptosis, failure, and could be implicated in the high incidence of lethal ventricular arrhythmias associated with these conditions. However, the cellular and molecular mechanisms of aldosterone action on cardio-myocytes are far from being completely elucidated. Moreover, the ability of MR to bind glucocorticoids with the same affinity as aldosterone, and the lack of protection of the receptor in cardiomyocytes against glucocorticoid exposure, render the interpretation of the relative pathophysiological role of mineralo- and gluco-corticoids quite complex. While glucocorticoids are classically considered as cardio-protective, partly due to the fact that they are able to antagonize aldosterone action on MR, recent studies have revealed that, in particular situations, they could mimic rather than oppose the response to aldosterone. In the present article, evidences are reviewed for the involvement of MR in several cardiac dysfunctions, the putative mechanisms of MR activation by mineralo- and glucocorticoids are compared, and a particular aspect of corticosteroid action linked to the risk of ventricular arrhythmias is discussed. Finally, pathophysiological roles for a specific class of “fetal” calcium channels, re-expressed in response to corticosteroid activation as well as in various cardiopathies are proposed.