Abstract
The paper by Zhang et al. in this issue [1] is challenging some well established concepts regarding the actions of dofetilide and adds a new dimension to the discussion of whether we can/should target the Na/Ca exchanger (NCX) in treatment of heart failure. It therefore deserves some further scrutiny and needs to be discussed in a broad perspective. The key findings of Zhang et al. are that (1) dofetilide increases NCX currents when studied in isolation with all other ion currents blocked, (2) dofetilide increases contraction under voltage clamp pulses of fixed duration, excluding indirect effects via block of the delayed rectifier K current, IKr. The authors therefore propose that dofetilide has a positive inotropic, and lusitropic, effect by enhancing NCX activity. This raises a number of discussion points. Is dofetilide not the highly specific IKr blocker we thought?
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