NR3C1 and atrial fibrillation: The mechanisms that correlate the excess of cortisol with the onset of AF could be attributable to: (i) hyperactivation of mineralo- and glucocorticoid receptors [39]; (ii) direct effects on the cardiac excitation–contraction coupling by alteration of intracellular calcium levels by protein kinase C-dependent mechanisms [40]; (iii) effect on morphology and performance of cardiac muscle, including biventricular systolic dysfunction, altered left atrium ejection fraction, and dilated left atrium, which are predisposing conditions for development of AF [41].