An animal experimental study demonstrated that ZWD delayed the progression of CHF in rats and increased myocardial contractility in CHF rats to improve the symptoms of heart failure significantly by the means of regulating the levels of sFas and sFas-L in serum, and also affected the apoptosis of myocardial cells in CHF rats.[11] Another experiment found that ZWD improved cardiac function in CHF rats by reducing Bax expression in cardiomyocytes and counterpoising Bcl-2 and Bax.[12]. This evidence concerns the gene BAX and congestive heart failure.