Abstract
Heart failure (HF) is a devastating disease and despite advances in medical therapy, mortality remains high due to ventricular arrhythmias. Modifications to the cardiac ryanodine receptor (RyR2) due to stress induced mechanisms ultimately lead to pathological Ca2+ leak during diastole, resulting in delayed after depolarisations and ventricular arrhythmias. Phenytoin, a hydantoin derivative used as an anti-convulsant, is known to exhibit weak Na+ channel blockade in cardiomyocytes. Recent studies revealed that phenytoin inhibits diastolic but not systolic Ca2+ leak from RyR2 channels of human failing hearts and has no effect on Ca2+ release from RyR2 channels from non-failing hearts [1].
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