The results showed: (1) IKr inhibition and INaL enhancement played crucial roles in the prolongation of action potential and generation of EAD in HF; (2) SERCA(PJup) inhibition and Jleak_JSR contributed most to the loss of calcium and active tension amplitudes in HF; (3) SERCA suppression was the biggest cause for the diastolic calcium and tension elevation; (4) SERCA remodelling and CaMKII activation induced alternans generation in failing myocytes. Here, CAMK2G is linked to hydrops fetalis.