ABSTRACT
Objective To explore the relationship of plasma NT-proBNP level and severity of chronic congestive heart failure (CHF) and investigate the curative effect and security of meglumine adenosine cyclophosphate (MAC) combined with perindopril on patients with CHF.Methods From June 2011 to June 2013,126 inpatients with chronic congestive heart failure were randomly divided into A group (42 cases,routine therapy),B group (41 cases,routine therapy and perindopril) and C group (43 cases,routine therapy and perindopril plus MAC),all cases treated for 14 days.The left ventricular ejection fraction (LVEF) and left ventricular end-diastolic diameter (LVEDD) by echocardiography and plasma NT-proBNP levels were evaluated before and after 14 days therapy.Results The plasma NT-proBNP levels in NYHA Ⅱ ～ Ⅳ classes were significantly difference compared each other between any two classes (P ＜0.05) and the levels was positively correlated with NYHA cardiac function class and LVEDD (r =0.617,P ＜ 0.01 ; r =0.412,P ＜ 0.01),negatively correlated with LVEF (r =-0.372,P ＜ 0.01).After 14 days therapy,compared with A group,the LVEF and LVEDD significantly improved (P ＜ 0.05) and NT-proBNP level significantly decreased (P ＜ 0.05) in B,C groups; Compared with B group,C group had lower NT-proBNP level (P ＜ 0.05) although no further improvement in cardiac function.Conclusions The plasma NT-proBNP level is correlated closely with the severity of CHF and it is a good examination of diagnose,therapy and evaluating prognosis of CHF.Perindopril may significantly decline plasma NT-proBNP level and improve cardiac function of CHF patients,combined with MAC may further decline plasma NT-proBNP level although not further improved LVEF.Giving MAC and perindopril to patients with CHF was secure and patients tolerated it well.
ABSTRACT
Objective To study the effects and mechanisms of myocardial injury in schistosome-infected mice.To investigate the effects and mechanisms of quercetin on myocardial injury due to the development of hepatic fibrosis after being treated by Praziquantel.Methods Eighty mice were divided into four groups:group A,group B,group C,and group D.Group A,group B,and group C were infected with Schistosoma japonicum cercariae.After 8 weeks,group A was treated with Praziquantel 500 mg/kg for 2 d,group B was treated with quercetin 30 mg/(kg?d) for 8 weeks after being treated with Praziquantel 500 mg/kg for 2 d.Group C was taken as experimental control without any treatment.Group D was taken as normal control.At the week 16,all mice were sacrificed and a part of liver tissue and myocardium tissue were preserved.HE Staining,electric microscope,RT-PCR,and immunohistochemical technique were applied to observing the changes of hepatic and cardiac histopathology,myocardial ultramicrostructure,the expression of myocardial c-fos,c-jun mRNA,and the contents of myocardial transforming growth factor-?1 (TGF-?1),typeⅠand typeⅢcollagen in mice infected with S.japonicum before and after treatments. Results There was different degree of myocardial injury among three groups of experimental control, Praziquantel treatment,Praziquantel combined with quercetin treatment.Praziquantel treatment relieved the degree of hepatic fibrosis and myocardial injury.The content of myocardial c-fos mRNA,c-jun mRNA,TGF-?1,typeⅠand typeⅢcollagen were obviously reduced compared to the experimental control. When Praziquantel treatment combined with quercetin,the degree of hepatic fibrosis and myocardial injury were further relieved.Although the content of myocardial c-fos mRNA,c-jun mRNA,TGF-?1, typeⅠand thypeⅢcollagen were still higher than those in normal control,those were reduced significantly compared to the group treated with Praziquantel.Conclusion Hepatic cirrhosis due to advanced schistosomiasis may lead to cardiac remodeling by stimulating the expression of immediate early gene and promoting the overexpression of TGF-?in myocardium.Anti-fibrosis therapy can reduce the degree of cardiac remodeling.Quercetin may protect myocardium through reducing the degree of hepatic fibrosis and inhibiting the expression of immediate early gene,which could decrease the level of myocardial TGF-?1.