Studies have indicated that dysfunction of NCX1, ryanodine receptor type 2 (RyR2) receptor dysfunction in cardiomyocytes leading to dysregulation of Ca2+ homeostasis will further cause mitochondrial dysfunction, defects in excitation-contraction coupling in cardiomyocytes, which will contribute to the development and maintenance of AF and HF (Lompré et al., 2010; Dridi et al., 2020). This evidence concerns the gene SLC8A1 and hydrops fetalis.