Atrial fibrillation (AF) is the most common complication after cardiac surgery and is responsible for significant morbidity and mortality. To assess whether preconditioning with renin-angiotensin-aldosterone system agents could limit myocardial tissue injury, we tested the force of contraction of human right atrial trabeculae during hypoxia-reoxygenation when exposed to aldosterone and/or potassium canrenoate.

We studied the effect of aldosterone and/or mineralocorticoid receptor (MR) antagonist potassium canrenoate administration prior to hypoxia-reoxygenation and in normoxic condition on force of contraction in 51 human right atrial trabeculae obtained from patients scheduled for coronary artery bypass surgery or aortic valve replacement. We also tested if adosterone exposure results in changes in levels of ERK1/2 phosphorylation.

The force of contraction of trabeculae was significantly reduced by aldosterone administration under normoxic or hypoxia-reoxygenation conditions. The rapid onset of this effect - 25 minutes - suggests a nongenomic mechanism. When compared with controls, potassium canrenoate by itself was not able to induce cardioprotection. However, coadministration of aldosterone and potassium canrenoate preconditioned isolated human atrial myocardium exposed to hypoxia - reoxygenation. This effect could be MR-dependent or not because both aldosterone and potassium canrenoate have some nongenomic MR-independent actions. Preliminary results showed that aldosterone exposure increased ERK1/2 phosphorylation levels.

Potassium canrenoate-induced cardioprotection prevents the deleterious effect of aldosterone on human atrial myocardial tissue. Further research required to determine the mechanism involved and the potential beneficial in clinical practice in order to reduce the incidence of postoperative atrial fibrillation.