Estrogen Has a Greater Impact on Cardiomyocyte Contractility in Atrial Fibrillation Than in Normal Sinus Rhythm

Estrogen plays a significant role in the regulation of cardiac contractility. Estrogen imbalance contributes to the development of atrial fibrillation (AF). The effect of estrogen on the functional remodeling of the atrial myocardium in AF has not been previously studied. We compared the effects of 50 and 100 nM 17β-estradiol (E2) on the contractility of atrial and ventricular cardiomyocytes in rats with paroxysmal AF. We found that in both hearts with normal sinus rhythm and hearts with AF, E2 modulates sarcomere contractility parameters primarily in ventricular cardiomyocytes. In hearts with normal sinus rhythm, E2 had a more pronounced effect on sarcomeric protein phosphorylation in ventricular cardiomyocytes than in atrial cardiomyocytes. In contrast, in AF, incubation with E2 had a greater effect on protein phosphorylation in atrial cardiomyocytes. The effects of E2 on the contractile characteristics of single cardiomyocytes were non-monotonic. These results indicate that estrogen significantly contributes to the remodeling of myocardial contractile function in AF, which is particularly important given the widespread use of hormone replacement therapy.