Objective: To discuss the curative efficacy of Yiqi Qiangxin decoction and influence on myocardial energy expenditure (MEE) and heart type fatty acid binding protein (H-FABP) in treating patients with chronic heart failure (CHF). Method: Eighty patients with CHF were randomly divided into western medicine group (40 cases) and observation group (40 cases) by random number table. Patients in western medicine group received 10 mg benazepril hydrochloride

50 mg metoprolol tablets

20 mg spironolactone tablets and 0.125 mg digoxin once daily. Based on the treatment of western medicine group

patients in observation group added 1 dose Yiqi Qiangxin decoction once daily. The patients in both groups received two 4 month periods of treatment. The New York Heart Association(NYHA) cardiac function class

6 minute walk test (6 MWT) and Lee's heart failure were observed. The left ventricular end-diastolic volume(LVEDV)

left ventricular end-systolic volume(LVESV) and left ventricular ejection fraction (LVEF) were detected using echocardiogram

and the MEE was calculated. Levels of serous N-terminal pro-brain natriuretic peptide (NT-proBNP) and heart type fatty acid binding protein (H-FABP) were detected before and after treatment. Data was analyzed by chi-square test of ordered data. Result: The score of NYHA cardiac function class in observation group was superior to that in western medicine group (P<0.05). After treatment

the score of Lee's heart failure in observation group was lower than that in western medicine group

and score of 6 MWT was obviously higher than that in western medicine group (P<0.01). The LVEDV

LVESV and MEE in observation group were obviously lower than those in western medicine group

while LVEF was significantly higher than that in western medicine group (P<0.01). Levels of NT-proBNP and H-FABP in observation group were lower than those in western medicine group (P<0.01). Conclusion: Yiqi Qiangxin decoction could alleviate the clinical symptoms and ameliorate cardiac function in patients with CHF

which may be chieved by regulating their MEE

blocking or reversing the myocardial remodeling.