TLX2 and hydrops fetalis: Given the importance of NCX in arrhythmogenesis via Ca2 + dependent mechanisms we would suggest that, on balance, the decrease in NCX current we see in this model of end-stage heart failure might mean that other mechanisms e.g. as a result of action potential shortening or K+ current remodelling, may be more important in increasing the susceptibility of the atria to arrhythmias in HF.