SLC4A3 and heart failure: Overall, our results suggest that alterations in Ca2+-handling or expression of Ca2+-handling proteins resulting from the loss of AE3, at least as it relates to direct modulation of the contractile apparatus, are unlikely to contribute to the reduction in rate-dependent inotropy or to the more rapid decompensation and heart failure observed in the HCM model (Al Moamen et al., 2011).