Purpose: Chronic volume overload to the heart has been suggested to generate arrhythmic substrates in the atria. We investigated whether aldosterone modifies inducibility of atrial fibrillation (AF) in rats with aorto-venocaval shunt (AVS).
Methods and Results: To elevate plasma aldosterone concentrations by 1.5 to 4.5-fold, aldosterone was intraperitoneally administered at 0.5, 1.0 or 1.5 µg/h for 4 weeks using an osmotic minipump that was implanted at the operation of AVS. Four weeks after the surgery, the duration of AF induced by burst pacing was 13±3 s in control AVS rats, whereas those in AVS rats receiving aldosterone at 0.5, 1.0 and 1.5 µg/h were 51±15, 75±18 and 99±34 s, respectively. The spontaneous premature atrial contraction often appeared in AVS rats receiving aldosterone, which was rarely observed in control AVS rats. There were no significant differences in the atrial effective refractory period, P-wave duration or atrial tissue weight among the all animal groups. Concomitant administration of spironolactone (100 mg/kg/day, p.o.) prevented the aldosterone-promoted AF.
Conclusions: Aldosterone enhanced stability of AF through mineralocorticoid receptors in the rat model of chronic volume overload. The results may partly reflect an increased risk of AF as observed in patients with primary aldosteronism.