Effects of Short-term High Dose Atorvastatin on Left Ventricular Remodeling in Patients with First Time Attack of Anterior Acute Myocardial Infarction

Objects The aim of this trial was to evaluate the effect of short-term high-dose atorvastatin therapy on levels of high-sensitivity C-reactive protein (hs-CRP), malonaldehyde (MDA), endothelin-1(ET-1), matrix metalloproteinases (MMPs), and left ventricular (LV) remodeling in patients with first time attack of acute anterior myocardial infarction (AAMI) . Methods A hundred and three patients with first time attack of AAMI who underwent successful primary percutaneous coronary intervention were randomized to receive atorvastatin 40 mg once daily for 1 week followed by 20 mg once daily (intensive treatment group, IT group, n=49), or atorvastatin 20 mg once daily (standard treatment group, ST group, n=54). Plasma levels of hs-CRP, MDA, ET-1, MMP-2 and MMP-9 were measured on admission, at 1 week, 2 weeks and 6 months follow up and compared between the IT group and ST group. Echocardiography was performed on admission, at 2 week, and 1 year follow up. The left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV) and left ventricular ejection fraction (LVEF) were measured at each echocardiographic examination and compared between the IT group and ST group. Results Plasma levels of hs-CRP (F=7.718, P=0.009), ET-1 (F=7.882, P=0.006), MMP-9 (F=4.834, P=0.028) and pro-BNP (F=4.603, P=0.032) were significantly lower at 1 week after initial onset of AAMI in the IT group compared with the ST group. The changes of LVEDV, LVESV, and LVEF at the 1 year follow-up from the admission did not differ between the IT group and the ST group (t=0.722, P=0.444; t=1.228, P=0.221;t=1.354,P=0.187, repectively). Conclusions Short-term high-dose atorvastatin treatment for AAMI was associated with lower hs-CRP, ET-1 and MMP-9 levels compared to the standard dose treatment. However, this beneficial effect is not likely to related to the left ventricular remodeling.     

Impact of 1, 25-(OH)2D3 on Left Ventricular Hypertrophy in Type 2 Diabetic Rats

Objective To investigate the impact of 1, 25-(OH)2D3 on left ventricular hypertrophy (LVH) in type 2 diabetic rats.
Methods Type 2 diabetic mellitus (DM) model rats were established by intraperitoneally injecting with 30 mg/kg streptozotocin. After 8 weeks, 19 male rats were identified as diabetic with left ventricular hypertrophy (LVH) by ultrasound examination, and randomly assigned into three groups:untreated (DM-LVH, n=7), treated with insulin (DM-LVH+INS, n=6), and treated with 1, 25-(OH)2D3 (DM-LVH+VD, n=6). Healthy male rats were used as the controls group (n=6). The fasting blood glucose and the insulin level were determined weekly. The left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor level were determined by 4 weeks later.
Results In the DM-LVH model group, the insulin level was significantly decreased compared with the non-diabetic control group (P<0.05), whereas the blood glucose, left ventricular mass index, myocardial collagen content, collagen volume fraction, and 1, 25-(OH)2D3-receptor expression were significantly increased (all P<0.05). In the DM-LVH+INS and DM-LVH+VD groups, the insulin levels were significantly increased compared with the DM-LVH model group (P<0.05), whereas the other parameters were significantly decreased (all P<0.05).
Conclusion 1, 25-(OH)2D3 could reverse LVH in diabetic rats and that the mechanism may involve stimulating insulin secretion and reducing blood glucose via direct up-regulation of 1, 25-(OH)2D3-receptor expression.     

Effects of Tongguan Capsule(通冠胶囊)on Post-myocardial Infarction Ventricular Remodeling and Cardiac Function in Rats

<正>Objective:To observe the effects of Tongguan Capsule(通冠胶囊,TGC) on post-myocardial infarction ventricular remodeling and heart function in rats.Methods:A rat model of acute myocardial infarction (AMI) was established by coronary ligation.Experimental rats were randomized to 4 groups including three model groups(Group A:captopril 5 mg/kg·day,n=7;Group B:TGC 10 g/kg·day,n=7;and Group C:placebo, n=8),and a sham-control group(Group D:blank control,n=6).Animals were treated for 4 weeks.The cardiac function of rats was assessed at the end of the experiment based on left ventricular ejection fraction(LVEF) and left ventricular short axis fractional shortening(LVFS) detected by colored echocardiography;meanwhile, the condition of ventricular remodeling was observed through the levels of left ventricular mass(LVM),plasma aldosterone(ALD),myocardial angiotensinⅡ(AngⅡ) and myocardial collagen measurements.Results:At the end of the experiment,LVEF and LVFS in Group A and B were improved significantly,while those in Group C were unchanged,the LVEF in Group A,B,C,and D was 0.57±0.46,0.61±0.08,0.36±0.55 and 0.76±0.02,respectively;and their LVFS was 0.31±0.52,0.34±0.04,0.23±0.57 and 0.45±0.03,respectively.The difference was statistically significant when comparing the two indexes in Group A and B with those in Group C and D(P0.05).LVM,levels of plasma ALD and myocardial AngⅡwere lower in Group A and B than in Group C,but a comparison between Group A and B showed an insignificant difference in lowering LVM and ALD,while the lowering of AngⅡwas more significant in Group B than in Group A(754.7±18.7 pg/mL vs 952.6±17.6 pg/ mL,P0.05).Morphological examination showed that in Group A and B the swollen myocardial cells had shrunk, with regularly arranged myocardial fibers and decreased collagen proliferation,but the improvements in Group B were more significant.Conclusion:TGC could markedly improve the post-infarction ventricular remodeling and cardiac function in rats,showing that the efficacy was better than or equal to that of captopril.     

Effects of Combined Therapy of Xuezhikang Capsule(血脂康胶囊)and Valsartan on Hypertensive Left Ventricular Hypertrophy and Heart Rate Turbulence

<正>Objective:To observe the effect of combined therapy with Xuezhikang Capsule(血脂康胶囊,XZK) and Valsartan on left ventricular hypertrophy(LVH) and heart rate turbulence(HRT) in hypertensive patients. Methods:Ninety primary hypertensive patients with LVH were randomly assigned to three groups.Basic treatment,including aspirin,β-blockers,calcium antagonists,etc.were administered to all patients.Additionally, Valsartan(VS,80 mg once a day) was given to the 30 patients in the VS group.Valsartan(in the same dosage) and XZK(600 mg,twice a day) were given to the 32 patients in the Chinese medicine(CM) group,while none was given to the 28 patients in the control group.The therapeutic course lasted for 24 months.Changes in left ventricular mass index(LVMI) measured by cardiac ultrasonic indices,HRT parameters,including the original heart rate(TO) and slope coefficient(TS),systolic and diastolic blood pressures(SBP and DBP),as well as blood cholesterol level(TC) were measured before and after treatment.Results:After treatment,TO and LVMI were lowered,while TS increased in both the VS group and the CM group(P0.01),but changed insignificantly in the control group.Significant differences between the CM group and the control group were shown in terms of TO,LVMI,SBP,DBP and TS(P0.01);and between the CM group and the VS group in terms of TO,LVMI and TS(P0.01).Moreover,HRT parameters showed an evident correlation with LVMI(r=0.519-0.635,P0.01). Conclusion:Combined therapy with XZK and Valsartan can improve hypertensive LVH and HRT parameters, and lessen the damage on the autonomous nervous system.     

Apoptosis, myocardial fibrosis and angiotensin Ⅱ in the left ventricle of hyp ertensive rats treated with fosinopril or losartan

Objective To investigate the different effects of an angiotensin Ⅱ type 1 (AT(1)) receptor antagonist, losartan, and an angiotensin converting enzyme (ACE) inhibitor, fosinopril, on cardiomyocyte apoptosis, myocardial fibrosis, and angiotensin Ⅱ (AngⅡ) in the left ventricle of spontaneously hypertensive rats (SHRs). Methods SHRs of 16-week-old were randomly divided into 3 groups: SHR-L (treated with losartan, 30 mg·kg(-1)·d(-1)), SHR-F (treated with fosinopril, 10 mg·kg(-1)·d(-1)), and SHR-C (treated with placebo). Each group consisted of 10 rats. Five rats, randomly selected from each group, were killed at the 8th and 16th week after treatment. Cardiomyocyte apoptosis, collagen volume fraction (CVF), perivascular collagen area (PVCA) and AngⅡ concentrations of plasma and myocardium were examined. Results Compared with the controls at the 8th and 16th week, systolic blood pressures were similarly decreased in both treatment groups. Left ventricular weight and left ventricular mass indexes were significantly lower in both treatment groups. However, the latter parameter at the 16th week was reduced to a less extent in the fosinopril group than that in the losartan group. Compared with the controls, cardiomycyte apoptotic index was significantly reduced at the 8th week only in the fosinopril group, and at the 16th week in both treatment groups. The index of the fosinopril group was lower than that of the losartan group at the latter endpoint examined. Compared with the controls, the left ventricular collagen volume fraction and perivascular collagen area at the 8th and 16th weeks were significantly reduced in the SHRs treated with either fosinopril or losartan. However, the collagen volume fraction at the latter endpoint in the fosinopril group was lower than that in the losartan group. Compared with the controls at endpoints, plasma and myocardium Ang Ⅱ levels were significantly increased in the losartan group. However, plasma Ang Ⅱ concentrations were not altered, and myocardium AngⅡ concentrations at the 8th and 16th weeks were significantly reduced in the fosinopril group. Conclusions Both losartan and fosinopril could effectively inhibit cardiomyocyte apoptosis and myocardial fibrosis and reverse heart hypertrophy. Fosinopril may be more effective in these cardioprotective effects, suggesting that the effects of both drugs are related to the inhibition of myocardium renin-angiotension-aldsterone system.     

Effect of oxidative stress on ventricular arrhythmia in rabbits with adriamycin-induced cardiomyopathy

The purpose of the present study was to examine the effects of oxidative stress on ventricular arrhythmias in rabbits with adriamycin-induced cardiomyopathy and the relationship between oxidative stress and ventricular arrhythmia. Forty Japanese white rabbits were randomly divided into four groups (n=10 in each): control group, metoprolol (a selective β1 receptor blocker) group, carvedilol (a nonselective β blocker/α-1 blocker) group and adriamycin group. Models of adriamycin-induced car-diomyopathy were established by intravenously injecting adriamycin hydrochloride (1 mg/kg) to rabbits via the auri-edge vein twice a week for 8 weeks in the adriamycin, metoprolol and carvedilol groups. Rabbits in the control group were given equal volume of saline through the auri-edge vein. Rabbits in the metoprolol and carvedilol groups were then intragastrically administrated metoprolol (5 mg/kg/d) and carvedilol (5 mg/kg/d) respectively for 2 months, while those in the adriamycin and control groups were treated with equal volume of saline in the same manner as in the metroprolol and carvedilol groups. Left ventricular end diastolic diameter (LVEDd) and left ventricular ejection fraction (LVEF) were measured by echocardiography. Plasma levels of N-terminal pro B-type natriuretic peptide (NT-proBNP), malondialdehyde (MAD) and superoxide dismutase (SOD) were detected. The left ventricular wedge preparations were perfused with Tyrode’s solution. The transmural electrocardiogram, transmural action potentials from epicardium (Epi) and endocardium (Endo), transmural repolarization dispersion (TDR) were recorded, and the incidences of triggered activity and ventricular arrhythmias were obtained at rapid cycle lengths. The results showed that TDR and the serum MDA and NT-proBNP levels were increased, and LVEF and the serum SOD level decreased in the adriamycin group compared with the control group. The incidences of triggered activity and ventricular arrhythmia were significantly higher in the adriamycin group than those in the control group (P<0.05). In the carvedilol group as compared with the adriamycin group, the serum SOD level and the LVEF were substantially increased; the TDR, and the serum MDA and NT-proBNP levels were significantly decreased; the incidences of triggered activity and ventricular arrhythmia were obviously reduced (P<0.05). There were no significant differences in the levels of MDA and SOD, LVEF, TDR and the incidences of triggered activity and ventricular arrhythmia between the adriamycin group and the metoprolol group. It was concluded that carvedilol may inhibit triggered activity and ventricular arrhythmias in rabbit with adriamycin-induced cardiomyopathy, which is related to the decrease in oxygen free radials.     

Therapeutic Mechanism of Yuxingeng Liquid(愈心梗液)on Early Ventricular Remodeling with Acute Myocardial Infarction in Rats

Objective:To examine the the therapeutic mechhanism of Yuxingeng liquid(愈心梗液,YXGL)On early ventricular remodeling in Wistar rats with acute myocardial infarction(AMI).Methods:Measur-ing the cardiac index(CI),left ventricular weight(LVW)and cardiac myocyte dimension and observingthe concentration of endothelin(ET)and angiotensin Ⅱ(AngⅡ)in the plasma and myocardium.AMImodels were established by ligature of left anterior descending coronary artery and the rats with AMI wererandomly divided into 6 groups:the model group,sham-operation group,captopril group,high dosageYXGL group,middle dosage YXGL group and low dosage YXGL group.From the next day after model-ing,the rats had been given YXGL through the gastric tube,which lasted for 4 weeks.And then,CI,LVW and concentration of ET and AngⅡ in the plasma and myocardium were tested.Results:Comparingwith model control group,high dosage YXGL,middle dosage YXGL andcaptopril can all significantly re-duce CI,LVW,cardiac cell dimension and content of ET and Ang     

Surgery for left ventricular aneurysm after myocardial infarction: techniques selection and results assessment

Background  The most appropriate surgical approach for patients with post-infarction left ventricular (LV) aneurysm remains undetermined. We compared the efficacy of the linear versus patch repair techniques, and investigated the mid-term changes of LV geometry and cardiac function, for repair of LV aneurysms.

Methods  We reviewed the records of 194 patients who had surgery for a post-infarction LV aneurysm between 1998 and 2010. Short-term and mid-term outcomes, including complications, cardiac function and mortality, were assessed. LV end-diastolic and systolic dimensions (LVEDD and LVESD), LV end-diastolic and end-systolic volume indexes (LVEDVI and LVESVI) and LV ejection fraction (LVEF) were measured on pre-operative and follow-up echocardiography.

Results  Overall in-hospital mortality was 4.12%, and major morbidity showed no significant differences between the two groups. Multivariate analysis identified preoperative left ventricular end diastolic pressure >20 mmHg, low cardiac output and aortic clamping time >2 hours as risk factors for early mortality. Follow-up revealed that LVEF improved from 37% pre-operation to 45% 12 months post-operation in the patch group (P=0.008), and from 44% pre-operation to 40% 12 months postoperation in the linear group (P=0.032). In contrast, the LVEDVI and LVESVI in the linear group were significantly reduced immediately after the operation, and increased again at follow-up. However, in the patch group, the LVEDVI and LVESVI were significantly reduced at follow-up. And there were significant differences in the correct value changes of LVEF and left ventricular remodeling between linear repair and patch groups.

Conclusions  Persistent reduction of LV dimensions after the patch repair procedure seems to be a procedure-related problem. The choice of the technique should be tailored on an individual basis and surgeon’s preference. The patch remodeling technique results in a better LVEF improvement, further significant reductions in LV dimensions and volumes than does the linear repair technique. The results suggest that LV patch remodeling is a better surgical choice for patients with post-infarction LV aneurysm.

     

A comparative study on the effects of low dose of tPA and differentregimens of intravenous urokinase in acute myocardial infarction

Objective　To compare the effects of low dose of recombinant tissue-type plasminogen activator(tPA) with those of conventional dose of urokinase (UK) and assess the influence of different regimens of intravenous UK in patients with acute myocardial infarction (AMI). Methods　Eighty patients with AMI were randomized to 50 mg of tPA (Group Ⅰ; n=26) using an accelerating approach or 1.0-1.5 million U of UK (Group Ⅱ; n=54). UK was administered as a single bolus injection of whole dose (Group Ⅱa; n=26) or half dose bolus injection followed by half dose infusion (Group Ⅱb; n=28). All patients underwent coronary arteriography 90 min after the initiation of intravenous thrombolysis, and the infarct-related coronary artery (IRA) patency was evaluated. Cardiac events during hospitalization were recorded and predischarge left ventricular function was determined by two-dimensional echocardiography. Results　The IRA patency rate was significantly higher in Group Ⅰ (88.4%) than in Group Ⅱ (53.7%) (P&lt;0.01). Group Ⅰ patients had less cardiac events during hospitalization (11.5% vs 33.3%) and greater improvement in left ventricular function than Group Ⅱ patients. However, these angiographic, left ventricular functional and prognostic parameters did not significantly differ between Group Ⅱa and Group Ⅱb. Conclusions　Thrombolysis after AMI with low dose of intravenous tPA exerts better angiographic and clinical effects than that with conventional dose of UK. The thrombolytic effects of UK were not affected by different regimens of intravenous administration of the agent.     

Effect of Salvia Miltiorrhiza Bge on Left Ventricular Hypertrophy and the Expression of Tumor Necrosis Factor-α in Spontaneously Hypertensive Rats

The effects of salvia miltiorrhiza Bge (SMB) on left ventricular hypertrophy (LVH) and the expression of tumor necrosis factor-α (TNF-α) in the left ventricle of spontaneously hypertensive rats and the action mechanism were investigated. Normal Wistar-kyoto (WKY) rats were used as negative control, and spontaneously hypertensive rats (SHR) were randomly assigned to receive pla- cebo or SMB. SMB (1 g/kg·d) was injected intraperitoneally for 12 weeks. Systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured. HE, VG and immunohistochemical staining combined with computed morphometry were employed to evaluate the cardiomyocyte size, diameter, the collagen volume fraction (CVF), perivascular circumferential area (PVCA), and tumor necrosis factor-α (TNF-α) expression in the left ventricular tissue. The results showed, as compared with WKY rats, the SBP, LVMI, cardiomyocyte size, diameter, CVF, PCVA, and TNF-α expression were increased markedly in the 20-week-old spontaneously hypertensive rats. SMB decreased LVMI (P<0.01), size of cardiomyocytes (P<0.01), collagen volume fraction (P<0.01), perivascular circum- ferential area (P<0.01), and TNF-α expression (P<0.01), but had no effect on SBP (P>0.05). It was suggested that chronic administration of SMB could inhibit and reverse the development of LVH in spontaneously hypertensive rats independent of BP. TNF-α may be involved in the reversal mecha- nism of LVH by SMB.     

Left ventricle geometry remolding after heart transplantation: A two-dimensional ultrasound study

The function of the transplanted heart will be affected by acute allograft rejection, chronic rejection, high blood pressure and so on, which may induce the reconstruction of the left ventricle and the increase of left ventricular mass （LVM）, and eventually lead to left ventricular hypertrophy that will significantly affect the prognosis of heart transplantation （HT）. The purpose of this study was to dy- namically monitor the changes of left ventricular geometric patterns after HT using two-dimensional echocardiography and to understand the remodeling process and its possible influencing factors. The left ventricular internal diameter, interventricular septal wall thickness, posterior wall thickness at end dias- tole were measured and the relative wall thickness （RWT）, left ventricular mass, left ventricular mass index were calculated respectively in 34 HT patients and 34 healthy volunteers by two-dimensional echocardiography. The type of left ventricular geometry was identified based on the echocardiographic determination of LVM index （LVMI） and RWT. The HT patients were divided into three groups ac- cording to the time length after surgery： A （3 months postoperatively）, B （6 months postoperatively） and C （12 months postoperatively）. We compared the parameters of left ventricle between HT group and normal control group, and explored the risk factors causing the increase of LVM. The results showed that 4 patients （16%） in group A had concentric remodeling. Nine patients （34.62%） in group B had re- construction, including 5 cases of concentric remodeling, 2 cases of concentric hypertrophy and 2 cases of eccentric hypertrophy. The hypertrophy incidence rate was 15.4% in group B. 15 patients （62.5%） had reconstruction in group C, including 9 cases of concentric remodeling, 5 cases of concentric hyper- trophy, and 1 case of eccentric hypertrophy. The prevalence of hypertrophy was 25%. Multivariate analysis showed that hypertension and acute rejection history were the risk factors that resulted in left ventricular hypertrophy. It is concluded that the left ventricular remodeling occurs following cardiac transplantation at an early stage and the incidence of left ventricular hypertrophy increases with survival time. In this study, the one-year prevalence of left ventricular hypertrophy was 25% after surgery. Hy- pertension and acute rejection history are risk factors that can predict the left ventricular hypertrophy.     

Angiotensin Ⅱ induced upregulation of Gαq/11, phospholipase Cβ3 and extracellular signal-regulated kinase 1/2 via angiotensin Ⅱtype 1 receptor

Background The role of the Gαq/11-mediated signal transduction pathway in angiotensin Ⅱ (Ang Ⅱ) induced cardiac hypertrophy remains unclear. This study was to investigate the role of the Gαq/11 signal transduction pathway in the development of cardiac hypertrophy in 2K1C hypertensive rats and in cultured neonatal rat ventricular myocytes (NRVMs) and to elucidate the effects of the pathway on Ang Ⅱ induced cardiac hypertrophy.Methods Renal hypertension was induced in 2K1C hypertensive rats by placing a silver clip around the left renal artery. At 8 weeks after operation, the systolic blood pressure, the ratio of left ventricular weight to body weight (LV/BW), and the concentration of AngⅡ in the heart were measured. The protein levels of Gαq/11 and extracellular signal-regulated kinase 1/2 (ERK1/2) were assayed by Western blot analysis, and the activity of phospholipase C (PLC) in the myocardium was detected using ［3H］-PIP2 as a substrate. Changes in ［3H］-leucine incorporation and in the protein levels of the signal molecules Gαq/11, PLCβ3, and ERK1/2 were measured after NRVMs were stimulated with 10-7mol/L AngⅡ.Results The protein levels of Gαq/11 and ERK1/2 in the hearts of 2K1C rats increased by 35.8% and 31.9%, respectively, compared with the sham group. The PLC activity in the 2K1C group was also significantly increased (P&lt;0.05). The levels of Gαq/11, PLCβ3, and ERK1/2 increased significantly after NRVMs were stimulated by AngⅡ. The upregulation of Gαq/11, PLCβ3 and ERK1/2 in NRVMs occurred prior to ［3H］-leucine incorporation increases, and could be inhibited with losartan. Conclusion AngⅡ can initiate cardiac hypertrophy and upregulate signal molecules in the Gαq/11-mediated signal transduction pathway, such as Gαq/11, PLCβ3 and ERK1/2, at both tissue and cellular levels.     

Effect of ETA receptor antagonist BQ-123 on cardiac function and endothelin system after coronary microembolization in rats

Objective To evaluate the effects of BQ-123 on cardiac function and ventricular remodelling after coronary microembolization (CME) in rats. Methods We created a rat model of CME by injecting a suspension of autogenic microthrombotic particles into left ventricle. Three days after the procedure, the 30 surviving rats were randomly divided into 3 groups, each consisted of 10 rats: sham-operation group(SO), CME model group(CM) and BQ-123 intervention group(BQ). Rats in the BQ group received BQ-123 (400μg/kg per day, intraperitoneally) for 4 weeks. Plasma and myocardial endothelin-1 (ET-1) were measured by radioimmunoassay. And serial echocardiography was performed to monitor alterations of left ventricular end-systolic and end-diastolic diameter (LVESD, LVEED), and left ventricular short-axis fraction shortening(LVFS) and ejection fraction (LVEF), and physiologicography to document the changes of left ventricular systolic pressure (LVSP) and end-diastolic pressure pressure(LVEDP), and left ventricular maximum positive and negative dp/dt (±LVdp/dtmax). Results Compared with sham-operated group, both LVEDD and LVESD were increased (P<0.01), whereas LVFS and LVEF were significantly decreased (P<0.01) in CME group; LVEDP was markedly increased, while LVSP and±LVdp/ dtmax markedly reduced in CME group (P<0.01); plasma and tissue ET-1 levels increased in CME group (P<0.01). BQ-123 intervention significantly decreased both the plasma and tissue ET-1 levels (P<0.01), and markedly increased LVFS and LVEF, with significant improvement of LVSP and±LVdp/ dtmax (P<0.01). Conclusions Treatment with BQ-123 prevents ventricular remodeling after CME due to suppression of the endothelin system.     

Effects of Yixin Jiangya Capsules on Insulin Resistance and Tumor Necrosis Factor-α in Cases of Primary Hypertension with Left Ventricular Hypertrophy

Objectives: To observe the effects of Yixin Jiangya Capsules (益心降压胶囊 capsules for nourishing the heart and lowering blood pressure) on insulin resistance (IR) and tumor necrosis factor-α (TNF-α) in patients with primary hypertension with left ventricular hypertrophy (LVH). Methods: Totally 93 cases were randomly divided into a control group of 31 cases taking Enalapril and a treatment group of 62 cases taking Enalapril and Yixin Jiangya Capsules. Results: Fasting serum insulin (FSI) and TNF-α obviously increased and insulin sensitive index (ISI) significantly decreased in both groups before treatment as compared to those of a healthy group. After treatment, FSI, TNF-α and fasting blood glucose (FBG) obviously decreased and ISI remarkably increased in the treatment group, while ISI significantly increased and TNF-α obviously decreased in the control group. The curative effect in the treatment group was remarkably superior to that in the control group. FSI was positively related to TNF-α before treatment in both groups. Conclusion: FSI and TNF-α obviously increase and ISI significantly decreases in patients with primary hypertension with LVH. FSI and TNF-α influencing each other are involved in the generation and development of hypertension. Yixin Jiangya Capsules can improve IR and decrease TNF-α.     

Inhibiting NF-κB increases cholesterol efflux from THP-1 derivedfoam cells treated with Angll via up-regulating the expression of ATP-binding cassette transporter A1

Objective:To study the role of nuclear factor-kappa B(NF- K B) in cholesterol efflux from THP-I derived-foam cells treated with Angiotensin Ⅱ (Ang Ⅱ ). Methods:Cultured THP-l derived-foam cells were treated with Ang Ⅱ or preincubated with tosyl-phenylalan inechloromethyl-ketone(TPCK) NF-K B inhibitor. The levels of activated NF-K B in the cells were examined by sandwich ELISA. Cellular cholesterol content was studied by electron microscopy scanning and zymochemistry via fluorospectrophotometer and cholesterol efflux was detected by scintillation counting technique. ABCAI mRNA and protein were quantified by RT-PCR and Western blotting. Results:Addition of TPCK to the cells before Ang Ⅱ stimulation attenuated the response of NF- K B p65 nuclear translocation induced by Ang Ⅱ and showed no peak in foam cells group and caused a reduction in cholesterol content and an increase in cholesterol effiux by 24.1%(P < 0.05) and 41.1%(P < 0.05) respectively, when compared with Ang Ⅱ group. In accordance, the ABCAl mRNA and protein were increased by 30% and 19%(P< 0.05) respectively, when compared with Ang Ⅱ group. Conclusion:Ang Ⅱ can down- regulate ABCAI in THP-l derived-foam cells via NF- K B, which leads to less cholesterol effiux and the increase of cholesterol content with the consequence of the promotion of atherosclerosis.     

Speckle Tracking Echocardiography Assessment of Global and Regional Contraction Dysfunction in the Mice Model of Pressure Overload

Speckle tracking echocardiography(STE) has been applied to the evaluation of cardiac contraction dysfunction. However, there were few studies on alteration of global and regional STE parameters in the process of myocardial hypertrophy and heart failure. In this study, STE was applied to evaluate the global and regional cardiac function under heart failure and hypertrophy in the mice model of pressure overload. Adult mice were subjected to mild or severe aortic banding with a 25 Gauge(G) or 27 G needle. After surgery, STE and conventional echocardiography were used in the sham group(n=10), mild trans-aortic banding(TAB) group(n=14) and severe TAB group(n=10) for 8 weeks. The results showed that the mice subjected to severe TAB showed a significant change in fractional shortening(FS), left ventricular(LV) mass, and left ventricular end diastolic diameter(LVEDD)(P<0.05 for each). Meanwhile, there were no significant differences in FS and LVEDD between the sham group and mild TAB group during the experimental procedures(P>0.05 for both). STE analysis revealed that longitudinal strain(LS) was significantly decreased in the severe TAB group as compared with the sham and mild TAB groups(P<0.05 for both) from the postoperative week 1. LS in the mild TAB group was reduced as compared to the sham group(P<0.05). Radial strain(RS) and circumferential strain(CS) were significantly decreased in the severe TAB group as compared to the sham group and the mild TAB group(P<0.05 for both) from the postoperative week 1(P<0.05 for both). Compared to the sham group, CS in the mild TAB group maintained unchanged during the test period, and RS was reduced only on the postoperative week 6(P<0.05). Finally, regional contraction dysfunction was analyzed in both hypertrophic and failing myocardium in longitudinal and radial directions. It was found that LS was largest in the apex region and RS was smallest in the apex region in the healthy and hypertrophic myocardium. It was also found that compared to the sham group, only base longitudinal strain in the mild TAB group was decreased. Each of regional strain in the severe TAB group was uniformly depressed in radial and longitudinal directions. It is concluded that STE has provided a non-invasive and highly feasible way to explore the global and regional contraction dysfunction in hypertrophic and heart failure myocardium in the murine model of pressure overload.     

Changes in Plasma Angiotensin Ⅱ and Circadian Rhythm of Blood Pressure in Hypertensive Patients with Sleep Apnea Syndrome Before and After Treatment

Objective To explore the changes in plasma angiotensin II (Ang II) and circadian rhythm of blood pressure among hypertensive patients with sleep apnea syndrome (SAS) before and after continuous positive airway pressure (CPAP) or surgical treatment.Methods A total of 180 essential hypertension patients were enrolled in our study.The determination of plasma Ang II concentration,ambulatory blood pressure (ABP),and polysomnography (PSG) monitoring were performed before and 3 months after CPAP or surgical treatment.Results Patients were classified into three groups by their apnea-hypopnea index (AHI):essential hypertension group (EH group,n=72;AHI<5),essential hypertension with mild SAS group (EH+mild SAS group,n=60,5≤AHI<20),and essential hypertension with moderate and severe SAS group (EH+moderate-severe SAS group,n=48,AHI≥20).The concentrations of plasma AngⅡ in the above three groups were 13.42±3.27,16.17±3.82,and 18.73±4.05 ng/mL respectively before treatment,and AngⅡ concentration in EH patients combined with SAS was significantly higher than that in EH group (all P<0.05).After treatment the values in the latter two groups significantly decreased to 14.67±2.56 and 15.03±3.41 ng/mL respectively (P<0.05).The incidence of non-dipper blood pressure curve in EH patients was 31.9%,and those in hypertensive patients with mild SAS and moderate-severe SAS were 51.7% and 58.3%,respectively before treatment.The incidence of non-dipper blood pressure curve in the EH patients with mild SAS was significantly higher than that of patients with EH alone (P<0.05).After CPAP treatment or surgery,the incidence of non-dipper blood pressure curve in the two SAS groups was significantly decreased to 38.3% and 39.6%,respectively (P<0.05).Conclusions Ang II might play a role in blood pressure variability in patients with obstructive SAS.CPAP or surgical treatment can improve blood pressure disorder and decrease plasma Ang II level in patients with obstructive SAS.     

High-frequency ultrasound evaluation of effects of early treatment with metoprolol on myocardial inflammatory cytokine expression in rats with acute myocardial infarction

This study evaluated the effects of early treatment with β-adrenergic blocker metoprolol on ventricular remodeling and function after acute myocardial infarction (AMI) by using high frequency ultrasound.The relationship between the efficacy and the expression level of cardiac myocardial inflammatory cytokine was examined in rats.The rat model of AMI was induced by ligating the left ante-rior descending artery.The surviving rats were randomly assigned to two experimental groups:MI control (MI) group and MI metoprolol (MI-B) group,with the rats undergoing sham operation serving as normal control (Sham).MI-B group was given metoprolol for 4 weeks (refer to the CCS-2 protocol) and the other two groups received equal volume of saline via intragastric (i.g.) administation.The ventricular remodeling and function were evaluated by high frequency ultrasound 4 weeks after the treatment.Then all rats were sacrificed for pathological examination and immunohistochemistrical detection of inflammatory cytokines,including IL-1β,IL-6,IL-10 and TNF-α.Compared with the MI group,the left ventricular end-systolic dimension,end-diastolic dimension,end-systolic volume and end-diastolic volume of the MI-B group were significantly decreased (P<0.01),while the left ventricular anterior wall end-diastolic thickness,ejection fraction and fractional shortening were obviously increased (P<0.01).The conspicuous improvement in the left ventricular morphology and function was coincident with the markedly reduced TNF-α and IL-1β expression and the increased IL-10 expression.We are led to conclude that early metoprolol treatment for AMI can regulate myocardial inflammatory cytokine expression to improve cardiac function and the underlying mechanism might be that it decreases the level of pro-inflammatory cytokines and increases the level of its anti-inflammatory counterparts in cardiac myocytes.Our study also showed that echocardiography is a useful technique for the structural and functional assessment of left ventricle after acute my     

Effect of Astragalus Injection on Left Ventricular Remodeling in Aged Patients with Acute Early-stage Myocardial Infarction

Objective: To observe the effect of Astragalus Injection (AI) on left ventricular remodeling in aged patients with acute myocardial infarction (AMI). Methods: Patients with AMI were randomly divided into the AI group (46 cases) treated with AI and the control group (46 cases) treated conventionally. Left ventricular end-diastolic volume index (LVEDVI), left ventricular end-systolic volume index (LVESVI), anterior endocardial segmental length (ASL) and posterior endocardial segmental length (PSL) were all assessed by echocardiogram after 1 week and 4 weeks treatment. The cardiac systolic and diastolic functions were detected by nuclide gating cardiac blood pool imaging at the 4th week. Results: After four weeks' treatment, no obvious change of LVEDVI, LVESVI and ASL in the AI group was found, but these indexes increased significantly in the control group, with significant difference shown between the two groups (P<0. 05). As compared with the control group, the left ventricular ejection fraction (LVEF),