Key result
Estradiol concentration-dependently prolonged cardiac repolarization and increased susceptibility to sotalol-induced arrhythmias, whereas progesterone shortened repolarization at higher concentrations.
Why the study?
Do estradiol and progesterone have different modulating effects on cardiac repolarization and susceptibility to sotalol-induced arrhythmias in female rabbit hearts?
Do estradiol and progesterone have different modulating effects on cardiac repolarization and susceptibility to sotalol-induced arrhythmias in female rabbit hearts?
Estradiol and progesterone exert divergent effects on cardiac repolarization, with estradiol increasing and progesterone decreasing susceptibility to drug-induced arrhythmias in a female rabbit model.
These sex hormone effects should not yet alter arrhythmia management; animal data leave open human relevance and require clinical validation.
This study aimed to comparatively investigate the acute modulating effects of oestrogen and progesterone on the repolarization and the susceptibility of female rabbits to class III anti-arrhythmic agents. The acute influence of estradiol and progesterone on the cardiac repolarization and the drug sensitivity of the rapidly activating delayed rectifier K(+) channel to sotalol was comparatively studied in Langendorff-perfused rabbit hearts at pharmacological concentrations through recording of epicardial monophasic action potentials. In Langendorff-perfused rabbit hearts, estradiol (1-30 μm) concentration-dependently prolonged the monophasic action potential durations (MAPD(30) and MAPD(90) ) (P < 0.05); while the effects of progesterone on MAPD were biphasic: it prolonged MAPD(30) and MAPD(90) at lower concentrations (1-3 μm) but shortened MAPD(30) and MAPD(90) at higher concentrations (10-30 μm). Sotalol-induced prolongation of MAPD(90) was significantly less in the hearts pretreated with progesterone than those treated with estradiol (P < 0.05). The incidence of the pro-arrhythmic events induced by sotalol in the hearts pretreated with progesterone was also significantly lower than those pretreated with estradiol (P < 0.05). In conclusion, estradiol and progesterone have different modulating effects on cardiac repolarization: estradiol can concentration-dependently prolong the cardiac repolarization time and thus may reduce the repolarization reserve and increase the susceptibility of female rabbits to sotalol-induced arrhythmias, whereas progesterone may shorten the cardiac repolarization time at concentrations above 10 μm, thus protecting the heart from drug-induced arrhythmias.
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Cheng et al. (2011) studied Cardiac repolarization and susceptibility to arrhythmias. Estradiol and Progesterone vs. Baseline / Each other was evaluated on Monophasic action potential durations (MAPD30 and MAPD90) and incidence of sotalol-induced pro-arrhythmic events (p=<0.05). Estradiol concentration-dependently prolonged cardiac repolarization and increased susceptibility to sotalol-induced arrhythmias, whereas progesterone shortened repolarization at higher concentrations.
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