Extensive studies have suggested that alterations in calcium‐handling proteins, including ryanodine receptor 2 (RyR2), SR Ca2+‐ATPase 2a (SERCA2a), phospholamban (PLB), and sodium/calcium exchanger 1 (NCX1), contribute to changes in intracellular calcium transients and diastolic SR Ca2+ release that, in turn, lead to Ca2+‐triggered arrhythmogenesis in HF animal models.9, 25, 26, 27 Therefore, we next detected the protein expression of RyR2, SERCA2a, PLB, and NCX1 in each group. This evidence concerns the gene RYR2 and hydrops fetalis.