肺心胶囊对慢性肺源性心脏病合并慢性心衰患者心功能的影响研究

目的：观察肺心胶囊对慢性肺源性心脏病（肺心病）合并慢性心力衰竭患者心功能及血浆脑钠肽和高敏C反应蛋白水平的影响。方法：将120例肺心病患者随机分为观察组和对照组，均予常规抗炎、抗心衰治疗，观察组加服肺心胶囊，疗程8周。治疗前后用彩超测定心功能指标[左心室射血分数（LVEF）、左心室舒张末期内径（LVDd）]，ELISA法和散射比浊法测定血浆N一末端脑钠肽前体（NT—proBNP）、高敏C反应蛋白（HS—CRP）水平。结果：治疗后观察组总有效率明显高于对照组，心功能指标LVEF明显升高、LVDd明显下降，血浆NT．proBNP、HS—CRP水平均明显下降，P均〈0．05；观察组血浆NT—proBNP与LVEF呈负相关（r=-0．70，P〈0．05），与LVDd呈正相关（r=0．74，P〈0．05）；血浆HS—CRP水平与LVDd呈正相关（r=O．32，P〈0．05），与LVEF增加呈负相关（r=-0．376，P〈0．05）。提示肺心胶囊治疗慢性心衰效果确切，其主要作用机制为降低血浆NT—oroBNP、HS—CRP水平。

Feixin Capsule Research on cardiac function in patients with Chronicpulmonar yheart disease and chronic heart failure

Objective To observe the Chronicpulmonar yheart disease and Feixin Capsule on cardiac function in patients with chronic heart failure and plasma brain natriuretic peptide and high-sensitivity high-sensitivity C-reactive protein levels in. Methods 120 patients with chronic heart failure （CHF） were randomly divided into two groups and the control group are therefore correspondingly routine anti-failure treatment, observation group took Feirdn Capsule, treatment for 8 weeks. Measured before and after treatment with color Doppler tdtras6und cardiac function [left ventricular ejection fraction （LVEF）, left ventricular end-diastolic diameter （LVDd）], ELISA method and nephelometry determination of plasma N-terminal pro-brain natriuretic peptide （NT-proBNP） , high-sensitivity C-reactive protein （HS-CRP） levels. Results After treatment the observation group was higher than the total effective rate, heart function parameters LVEF increased significantly, LVDd decreased significantly, plasma NT.proBNP, HS-CRP were sign/ficantly decreased, P are ＂0.05; observation of plasma NT-proBNP and the LVEF was negatively correlated （r =- 0.70, P 〈0.05）, and LVDd was positively correlated （r = 0.74, P 〈0.05）; Plasma HS-CRP level and LVDd was positively correlated （r 2 0.32 P 〈0.05）, and the increase in LVEF was negatively correlated （r =- 0.376, P 〈0.05）. Tip Feixin Capsule precise effect of the treatment of chronic heart failure, the main mechanism to reduce plasma NT-proBNP, HS-CRP levels.