Objective: The purpose is to study the mechanism of Baihua Danshen decoction in treatment of coronary heart disease (CHD) from the view point of endothelial function. Method: Eighty-eight cases of patients were divided into control group (44 cases) and observation group (44 cases) according to the hospital sequence. Based on 'The guide to the diagnosis and treatment of chronic stable angina'

the patients in control group took conventional treatment

including anticoagulation

antihypertensive

fat adjustment and improvement of coronary blood flow. On the basis of control group

the patients in observation group took Baihua Danshen decoction

1 dose/day. The treatment course is 12 weeks. Ultrasound is used to evaluate the function of flow-mediated dilatation (FMD). The levels plasma total cholesterol (TC)

triglyceride (TG)

low density lipoprotein cholesterol (LDL-C)

high density lipoprotein cholesterol (HDL-C) were detected before and after treatment. Ria method is used to determine the levels of plasma endothelin-1 (ET-1)

thromboxane 2 (TXB2) and 6-ketone prostaglandin F1a (6-Keto-PGF1a). The nitrate reduction method is used to evaluate nitric oxide (NO) level. The times and duration of angina are recorded. Result: During the treatment

the times and duration of angina in observation group were less than the control group (P<0.05). After the treatment

the levels of TC

TG

LDL-C of both groups were decreased

while observation group is lower than the control group (P<0.01). The level of HDL-C of two groups was increased

while the observation group was higher than control group (P<0.01). The levels of TXB2

ET-1 and ET-1/NO ratio were declined after the treatment

while the observation group are lower than the control group (P<0.01). The levels of NO and 6-Keto-PGF1a were increased after the treatment

while the observation group was higher than control group (P<0.01). The improvement of FMD in observation group is better than that of control group (P<0.01). Conclusion: Baihua Danshen decoction can improve angina pectoris of patients with CHD and regulate fat metabolism. Its mechanism may be related to adjust the imbalance of ET/NO and TXB2/6-Keto-PGF1a state and improve vascular endothelial function of patients with CHD.