Objective To investigate the quality of life (QOL) of patients with frequent premature ventricular contractions (PVCs) and the effects of radiofrequency catheter ablation (RFCA) on them.Methods 120 patients with frequent PVCs,100 cases with frequent APCs and 60 healthy persons were assessed by 36-Health survey questionnaire (SF-36) originally.Three months later,the QOL of 48 cases received RFCA and 72 cases with drug therapy were evaluated again by SF-36.Meanwhile,decrease of PVCs were also calculated between these two groups.Results The scores of physiological function and mental health in patients with PVCs were lower than that of cases with APCs,while the score of bodily pain in patients with PVCs was higher (P value:0.0002-0.0380).In addition,the quality of life in patients with frequent PVCs were worse than healthy control(P value:0.0001-0.0915).Three months later,PVCs in 48 cases with frequent PVCs received RFCA were much fewer than that of 72 cases with drug therapy (t=18.8682,P＜0.01),and the quality of life in the former was much better than the latter (F=15.329-39.274,P＜0.01).Conclusion Frequent PVCs can deteriorate the patients' quality of life.RFCA can control or eliminate PVCs in these patients and markedly improve the quality of life of them.

Objective To study the impact of depression disorder in patients after coronary stent implantation on incidence rate of in-stent restenosis (ISR) in the coronary heart disease( CHD ), and its possible pathophysiological mechanisms. Methods According to the Hamilton Depression Scale (HAMD-24) and Self-rating Depression Scale(SDS) score,95 patients with unstable angina received coronary drug-eluting stent implantation combined with depression disorder were serve as the study group; randomly selecte 246 cases without depression due to unstable angina pectoris after coronary stent implantation as the control group in the same period. The incidence rate of ISR in these two group were observed, and serum aldosterone ( ALD), high-sensitivity C-reactive protein (hs-CRP) ,Leptin levels in two groups were compared. Results The incidence rate of ISR in study group were significantly higher than that of the control group (28/95 vs 46/246, P＜0. 05). Following with the aggravation of depression disorder,the incidence rate of ISR were elevated( χ2 =8. 148, P=0.017). Serum ALD,hs-CRP and Leptin levels of study group were significantly higher than the control group 7 days later after drug-eluting stent implantation ( ALD:277.4 ± 35.9 vs 258.9 ± 60.9, t= 3. 459, P= 0. 001; hs-CRP: 12.03 ± 3.06 vs 11.10 ±2. 806, t = 2.573, P = 0.008; Leptin:5.27 t 1.07 vs 4.98 ± 0.99, t= 2.323, P= 0.021 ). Pearson correlation analysis showed that its HAMA-24 score was positively correlated with serum ALD ,hs-CRP and Leptin( r=0.291,P=0.026; r=0.350, P=0.014; r=0. 312, P=0.023) ,and SDS score was positively correlated with hs-CRP( r=0. 302, P= 0. 020). Conclusion Serum ALD, hs-CRP and Leptin levels are higher in patients after coronary stent implantation combined with depression in patients, and the incidence rate of ISR is also higher in these patients, and the rates are elevated according to the aggravation of depression disorder.

Objective: To study the impact of astragaloside on ventricular remodeling and peroxisome proliferator activated receptor a (PPARa) expression in pressure-overload rats and to preliminarily explore its mechanism. Methods: Pressure-overload rat's model was established by abdominal aorta constriction (AAC) in 8-week old SD rats and the result was conifrmed by echocardiography at 6 weeks later. Pressure-overload rats were divided into 4 groups with different intragastric treatment: Model control (normal saline) group, Benazepril hydrochloride [10mg/(kg.d)] group, Low-dose astragaloside [40mg/(kg·d)] group and High-dose astragaloside [80mg/(kg.d)] group; in addition, Sham operation group, the rats received intragastricnormal normal saline.n=20 in each group and all animals were treated for 8 weeks. Rat's cardiac structure and function indexes were assessed by echocardiography, hemodynamic parameter was examined by left ventricular intubation, myocardium and blood levels of free fatty acid (FFA) were determined, morphological changes of myocardial tissue was observed by HE and Masson staining, mRNA and protein expressions of PPARa were measured by qRT-PCR and Western blot analysis. Results: Compared with Sham operation group, Model control group showed increased left ventricular mass index(LVMI), collagen volume fraction (CVF) and FFA level, allP<0.05, while decreased mRNA and protein expressions of PPARa, bothP<0.05. Compared with Model control group, Low-dose and High-dose astragaloside groups presented reduced LVMI, CVF and FFA level, allP<0.05-0.01, while elevated mRNA and protein expressions of PPARa, bothP<0.01. Conclusion:Astragaloside IV mayinhibit myocardial remodeling in pressure-overload rats, which might be via up-regulating mRNA and protein expressions of PPARa, enhance myocardiumFFA utilization, and therefore improve myocardial energy metabolism.

Objective: To observe the effects of astragaloside IV on myocardial fibrosis and connective tissue growth factor (CTGF) expression in experimental rats with chronic heart failure (CHF).
Methods: CHF model was established by abdominal aorta constriction (AAC) and the rats were divided into 5 groups:Sham operation group, the rats received normal saline 2 ml/day, n=10, CHF group, the rats received normal saline 2 ml/day, n=12;Astragaloside IV groups, CHF rats received astragaloside IV at (20, 40, 60) mg/kg respectively and n=12 in each group. All animals were treated for 4 weeks. Hemodynamic indexes were monitored, left ventricular mass index (LVMI) was calculated, morphologic changes of myocardial tissue was observed by HE staining, myocardial ifbrosis degree and collagen volume fraction (CVF) were measured by Masson staining. The mRNA and protein expressions of CTGF were detected by RT-PCR and immunohistochemistry, Western-blot analysis respectivety.
Results: Compared with CHF group, 3 Astragaloside IV groups had decreased LVMI and CVF, P<0.05-0.01;Astragaloside IV (40 and 60) mg/kg groups presented decreased LVEDP and LVSP, increased ±dp/dtmax, P<0.01 to P<0.05 and improved pathological morphology. Compared with Sham group, CHF group had increased average CTGF OD value (0.09 ± 0.03) vs (0.45 ± 0.04) and increased expression of myocardial CTGF (0.57 ± 0.06);compared with CHF group, the average CTGF OD values in Astragaloside IV (20, 40, 60) mg/kg groups were all decreased (0.39 ± 0.05), (0.30 ± 0.06), (0.24 ± 0.04) and decreased expressions of myocardial CTGF (0.44 ± 0.05), (0.35 ± 0.02), (0.28 ± 0.03) respectively, all P<0.01.
Conclusion: Astragaloside IV can inhibit myocardial ifbrosis and improve cardiac function in CHF rats, which might be via inhibiting the over expression of myocardial CTGF.

Objective To investigate the relationship between the plasma levels of ET-1,TAT,and hs-CRP and slow coronary flow syndrome (SCFS),and explore effects of coronary endothelial function,coagulation function,and inflammatory reaction on blood flow of coronary artery.Methods A total of 400 cases with normal blood flow of coronary artery by coronary angiogram was randomly selected.The coronary flow patterns were determined by corrected thrombolysis in myocardial infarction frame count method (cT-FC).Among them,45 cases whose average cTFC more than 27 were assigned as SCFS group,the other 45 cases no SCFS.Plasma levels of ET-1,TAT and hs-CRPwere examined with enzyme-linked immunosorbent assay (ELISA),and were compared between two groups.Moreover,multivariate analysis evaluating predictors of SCFS was performed with regression test.Results No statistical difference was found between two groups concerning the gender,history of hypertension,diabetes mellitus,and cigarette alcohol percentage..The plasma level of HDL in SCFS group was lower than that of no SCFS [(1.22 ± 0.42) mmol/L vs (1.44±0.34) mmol/L,t =-2.731,P ＜0.01],but the plasma level of glucose in the former was higher than that of the latter [(5.68 ±0.62) mmol/L vs (5.10 ±0.84) mmol/L,t =3.727,P ＜0.01].However,Plasma levels of ET-1,TAT and hs-CRP in SCFS were higher than that of no SCFS [(94.3 ± 16.78) ng/Lvs (83.5±12.53) ng/L,t =3.051,P ＜0.01;(12.96±3.24)μg/Lvs (8.76 ±2.64)μg/L,t =5.945,P ＜ 0.01 ; (2.48 ± 0.35) μg/L vs (1.38 ± 0.46) μg/L,t =11.259,P ＜ 0.01].Furthermore,Logistic regression analysis showed that ET-1,TAT and hs-CRP were risk factors for SCFS (OR ＞ 1.22).Conclusions Due to coronary endothelial dysfunction,endothelial inflammatory reaction,and activated coagulation function,slow coronary flow of coronary artery occurs.

AIM:To observe the effects of astragaloside IV (AS-IV) on myocardial fibrosis in chronic heart failure ( CHF) rats and to explore the underlying mechanism preliminarily .METHODS:Chronic heart failure model rats established by abdominal aorta constriction (AAC) were divided into CHF group, valsartan group and AS-IV group.Sham operation group was also established .The rats in valsartan group and AS-IV group received valsartan and AS-IV at 2 and 30 mg· kg-1 · d-1 , respectively.The rats in sham operation group and CHF group received normal saline .After 8 weeks of treatment, the cardiac structure and the hemodynamic parameters were measured .The morphologic changes of myocardial tissue were observed after staining .The expression of long-chain acyl-CoA dehydrogenase ( LCAD) and 6-phosphofructoki-nase-1 (PFK1) at mRNA and protein levels was determined by RT-qPCR and Western blot.RESULTS:Compared with sham operation group , left ventricular mass index ( LVMI) , collagen volume fraction ( CVF) , left ventricular posterior wall depth (LVPWD), and the mRNA and protein of PFK1 in CHF group were increased (P<0.05), while the mRNA and protein levels of LCAD were decreased (P<0.05).Compared with CHF group, the LVMI, CVF, LVPWD, and the mRNA and protein levels of PFK1 in valsartan group and AS-IV group were decreased (P<0.05), while the mRNA and protein levels of LCAD were increased (P<0.05).CONCLUSION:AS-IV inhibits myocardial fibrosis in the CHF rats , the mechanism of which might be associated with up-regulating the expression of LCAD , down-regulating the expression of PFK1 and normalizing the myocardial energy metabolism .

Ventricular myocytes from hearts of the neonatal SD rats were treated with 10-7,10-6,and 10-5 mol/L simvastatin for 72 hours under high glucose condition. Compared with control group,the viability of cadiomyocyte was significantly lower in high glucose group (P＜0.01 ).The activity of lactate dehydrogenase,the relative expressions of NADPH oxidase subunits p22phox,p47phox mRNA,and reactive oxygen species level in the high glucose group were higher than those of control group ( all P＜0.05).lndexes mentioned above were significantly improved by simvastatin treatment in a dose-dependent manner.These results suggest that simvastatin ameliorates high glucose-induced injury of cardiomyocytes via increasing the expression of NADPH oxidase mRNA.