Forced expression of STIM1 in cultured adult feline ventricular myocytes increased diastolic spark rate and prolonged AP duration.

In failing heart, AP morphology was dramatically altered, with a significantly elevated plateau potential and prolonged AP duration.

I(X1) showed steeper rectification, slower activation, and more rapid deactivation in hypertrophy myocytes, abnormalities which may contribute to the prolonged AP duration of hypertrophied myocardium.