Of note, cardiomyocyte apoptosis is well known to be an important pathologic changes in heart failure, and the present study indeed confirms that large amount of apoptotic cells in HF rats and ECH significantly reduces the apoptosis via regulating SIRTI/FOXO3a/MnSOD pathway and inhibiting mitochondrial oxidative stress, as mentioned above. This evidence concerns the gene SOD2 and hydrops fetalis.