Search

Endothelial progenitor cells (EPCs) contribute to the endogenous endothelial repair program during hypercholesterolemia. EPC count and migratory and proliferative capacities remain unchanged in the premenopausal female with hypercholesterolemia. However, the changes of count and activity of circulating EPCs in the hypercholesterolemic postmenopausal females are unknown. Here, we find that the migratory and proliferative capacities of circulating EPCs were decreased in patients with hypercholesterolemia versus normocholesterolemia. No significant differences were found between postmenopausal females and age-matched males. NO production showed positive correlation with the activity and count of circulating EPCs in patients with hypercholesterolemia. Flow-mediated dilatation (FMD) is directly interrelated with EPC counts and function. Our findings reveal that decreased EPC count and endothelial dysfunction lead to less NO production in hypercholesterolemic postmenopausal females. Maintaining the EPC numbers and activity might be emerging as a potential therapeutic strategy to reduce the risk of cardiovascular injury in elder women.

Endothelial progenitor cells (EPCs) have endogenous endothelium-reparative potential, but obesity impairs EPCs. Overweight premenopausal women have a normal number of circulating EPCs with functional activity, but whether EPCs in overweight postmenopausal women can repair obesity-related endothelial damage requires further investigation. For this purpose, we examined the function and number of circulating EPCs, evaluated vascular endothelial function, and explored the underlying mechanism. Compared with normal weight or overweight age-matched men, postmenopausal women (overweight or normal weight) had a diminished number of circulating EPCs and impaired vascular endothelial function, as detected by flow-mediated dilatation. Moreover, GTCPH I expression and the nitric oxide level in overweight postmenopausal women and men were significantly decreased. Together, our findings demonstrate that the number or function of circulating EPCs and endothelial function, which is partially regulated by the GTCPH I/BH4 signaling pathway, is not preserved in overweight postmenopausal women. The GTCPH I/BH4 pathway in circulating EPCs may be a potential therapeutic target for endothelial injury in overweight postmenopausal women.

To investigate the prevalence of diabetes and prediabetes and their association with the risk for coronary heart disease (CHD) in elderly residents in Haizhu District of Guangzhou.Stratified random sampling was employed to select a total of 1800 resident aged 50 years or older in the region. The fasting fingertip blood glucose5.6 mmol/L was used as the criterion for the initial screening. The data were collected from qualified subjects via scheduled questionnaire surveys, blood collection and testing, and physical examination. The subjects were divided into the 3 groups, namely normal blood glucose, prediabetes, and diabetes groups. The combination rates of the relevant risk factors (hypertension, hyperlipemia, obesity, and central obesity) were compared among the groups by Framingham Heart Study to predict the occurrence of CHD in 10 years.The incidence was 11.00% for prediabetes and 7.56% for diabetes in the elderly residents in Haizhu District. The occurrence of hypertension, hyperlipemia, obesity, and central obesity was significant higher in the prediabetes and diabetes group than in the normal blood glucose group, and showed no significant differences between the former two groups. The 10-year risks for CHD were markedly higher in both the prediabetes and diabetes groups than in the normal blood glucose group, but similar between the former two groups.Elderly patients with prediabetes and diabetes have significantly increased 10-year risk for CHD in comparison with those with normal blood glucose, but the risk is similar between the former two groups, indicating a close association of IGR (impaired fasting glucose+ impaired fasting glucose) with CHD. Early control of blood glucose is essential to the prevention and control of CHD.

To assess the value of biochemical marker detection in risk stratification in hospitalized patients with acute coronary syndrome (ACS).A total of 264 consecutive patients (180 male and 84 female patients) admitted for complaint of chest tightness or/and pain were evaluated for a decision of coronary angiography (CAG) within 24 h after admission. The patients were divided into two groups to receive emergency or elective CAG. The venous blood samples were taken from the patient immediately after admission for detection of amino-terminal pro-brain natriuretic peptide (NT-pro-BNP), high-sensitivity C-reactive protein (hs-CRP), myeloperoxidase (MPO), monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule (sICAM-1), soluble CD40 ligand (sCD40L), matrix metalloproteinase 9 (MMP-9), interleukin-6 (IL-6), interleukin 27 (IL-27) and creatine kinase isoenzyme (CK-MB) were detected.No significant differences in NT-proBNP, hs-CRP, MPO, sCD40L, and MMP-9 were found between emergency CAG group and elective CAG group (P0.05). Logistic regression identified significant differences in NT-proBNP, hs-CRP, MPO, IL-27 and CK-MB between the two groups, and a predictive model for risk stratification of ACS was established using these biomarkers. The ROC curves of this predictive model showed an area under the curve of 98.1, suggesting a high predictive value of this model in assessment of the changes or progression of ACS.Combined detection of the biochemical markers can be helpful for risk stratification of the hospitalized patients with ACS early after admission.

To compare the peripheral dendritic cell subpopulation changes in patients with or without coronary artery disease.A total of 60 patients with angiographic documented coronary artery disease (CAD) were recruited in this study, including 20 cases with acute myocardial infarction (AMI group), 20 cases with unstable angina(UA group) and 20 patients with stable angina (SA group). Eleven patients with chest pain and without coronary stenosis served as chest pain control (CPS group). Ten cases without heart diseases served as normal control (Normal control group). Numbers of peripheral myeloid dendritic cell (mDC) and plasmacytoid dendritic cell (pDC) precursors were determined by FACS.The proportions of mDC precursors were significantly lower in UA group and AMI group (4.7% +/- 2.6%, 5.0% +/- 2.7%) than that in SA, CPS and control groups (11.0% +/- 6.4%, 12.0% +/- 3.9%, 12.3% +/- 3.3%, respectively, all P0.001). pDC numbers were similar among groups.Reduced circulating mDC subsets in patients with unstable angina and AMI might suggest enhanced mDC recruitment to vulnerable plaques in these patients.

To observe the changes in the myocardial ultrastructure of diabetic rats and the effect of enalapril treatment.Male Wistar rats were divided into 3 groups, namely the control group, diabetic group and enalapril intervention group. Diabetes was induced with peritoneal injection of streptozotocin in the latter 2 groups, and in enalapril group, the rats were treated with enalapril at the daily oral dose of 2 mg/kg for 1, 3 and 5 months after streptozotocin injection. Histological analysis of the left ventricular tissue was performed with transmission electron microscope 1, 3, and 5 months after establishment of diabetes.Onset of myocardial damages was observed 1 month after the development of diabetes in the rats with gradual time-dependent exacerbation. Enalapril treatment could partially reverse the myocardial destruction in the diabetic rats.Enalapril intervention may improve the ultrastructural pathology of the myocardium in diabetic rats, which is suggestive of the action mechanisms of angiotensin-converting enzyme inhibitors in myocardium preservation.

To investigate the changes of CD4(+)CD28(-) T cell and CD4(+)CD25(+) regulatory T cell (Treg) subsets in patients with coronary artery disease (CAD).Twenty-eight patients with angiographically established CAD were recruited in this study, including 16 with unstable angina (UA group) and 12 with stable angina (SA group). Eleven patients with chest pain syndrome served as the control group. The proportions of peripheral CD4(+)CD28(-) T cells and CD4(+)CD25(+) Treg subsets were determined with fluorescence-activated cell sorting (FACS).The proportions of CD4(+)CD25(+) Treg were significantly lower in UA group (6.55-/+2.45%) than in SA (14.01-/+4.92%) and control groups (13.55-/+3.87%). The proportions of CD4(+)CD28(-) T cells were significantly higher in UA group (10.55-/+4.76%) than in SA (2.64-/+1.33%) and control (2.75-/+1.55%) groups.Alterations of circulating T-lymphocyte subsets occur in patients with UA. The changes of Treg and CD4(+)CD28(-) T cells may lead to breakdown of peripheral autoimmune tolerance and play an important role in the development and progression of CHD.

To observe the dynamic changes of plasma adrenomedullin (ADM) levels and the effect of enalapril intervention in diabetic rats.Fifty-two wistar rats were grouped into 1- and 3-month groups (7 each), both including a control and a streptozotocin-induced diabetic group. The 5-month group was divided into control, diabetic and enalapril-treatment diabetic groups (8 each, the last group receiving oral enalapril treatment at the daily dose of 2 mg/kg from the first to the fifth month after diabetes induction). Blood samples were collected from the heart of the rats at the end of 1, 3 and 5 months for determination of plasma ADM concentrations radioimmunoassay.Plasma ADM levels were significantly higher in diabetic rats than in the corresponding control rats in 1- and 3-month groups. ADM levels in the diabetic rats of 5-month group were significantly decreased in comparison with that of 1- and 3-month groups. In 5-month group, plasma ADM levels of enalapril-treated diabetic rats elevated significantly in comparison with that in the control rats and the diabetic rats without enalapril treatment.ADM may play an important role in the pathophysiology of diabetes.

To study the mechanism of urotensin II(U II)-stimulated adrenomedullin secretion in human vascular endothelial cells.In cultured human vascular endothelial cells (HEVCs), different concentrations of U II was used to stimulate the secretion of Adm, and different inhibitors were used to study the changes in the secretion after block of different signal transduction pathways. The contents of Adm in the medium were detected with radioimmunoassay.U II-stimulated Adm secretion in the HEVCs in a time- and concentration-dependent manner. Adm contents of the treatment groups were comparable with that of the control group (P0.05 ), and the secretion of Adm could be inhibited by the inhibitor of extracellular signal-regulated protein kinases (PD098059), p38 kinase inhibitor (SB202190), calmodulin inhibitor (W7) and Ca(2+) inhibitor (nicardipine)(P0.05), but calcineurin inhibitor and protein kinase C inhibitor (H7) had no such effect (P0.05).Ca(2+), MAPK, CaM-PK and p38 signal transduction pathways may play major roles in U II-stimulated secretion of Adm in HVECs.

To investigate the changes in plasma urotensin II(U II) expression levels in patients with coronary heart disease (CHD).Plasma U II levels in 50 CHD patients with coronary stenosis indicated by coronary angiography and 20 healthy subjects were determined by radio immunoassay.Venous plasma U II levels were significantly lowered in CHD patients in comparison with the healthy subjects (1.61+/-1.02 pg/ml vs 3.70+/-1.30 pg/ml, P=0.000). In the CHD patient group, significantly differences were noted in the U II levels between patients with stable angina (2.62+/-1.20 pg/ml), unstable angina (1.39+/-0.80 pg/ml) and acute myocardial infarction (AMI, 1.04+/-0.45 pg/ml, P=0.004). CHD patients with coronary artery occlusion and those with only coronary stenosis had comparable venous plasma U II levels (1.29+/-1.02 pg/ml vs 1.76+/-1.00 pg/ml, P=0.131), whereas the patients with restenosis after percutaneous transluminal coronary angioplasty (PTCA) had higher U II levels than the other subjects in the CHD patient group (2.28+/-0.94 pg/ml vs 1.40+/-0.96 pg/ml, P=0.008), and the femoral plasma U II levels were significantly elevated after PTCT, increasing from 1.18+/-1.14 pg/ml to a postoperative level of 2.22+/-1.77 pg/ml (P=0.001).U II might play a role in the pathophysiological process of CHD and can be involved in the restenosis after angioplasty.

To evaluate the short-term therapeutic effect of percutaneous transluminal coronary angioplasty (PTCA) with stent implantation in the treatment of myocardial infarction with severe pump failure.The clinical data of 73 patients receiving PTCA and stent implantation for myocardial infarction with severity pump failure were analyzed and grouped according the occurrence of complications, degree of the vascular lesions and the complexity of the surgical procedures. Preoperative and postoperative ventricular ejection fractions (LVEF) were compared in each case.The degree of vascular lesions and surgical complexity were not shown to relate to the occurrence of the complications. Except in cases complicated by chronic renal dysfunction, significant improvement was achieved in the patients 7 d after the operation (P0.05), regardless of different degrees of vascular lesions and surgical complexity.PTCA with stent implantation is effective to improve the short-term cardiac function of patients with myocardial infarction and severe pump failure.

To study the value of detecting high-sensitivity C-reactive protein (hs-CRP) combined with determination of total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C) in the diagnosis of coronary artery disease (CHD).A total of 240 patients with documented CHD and 40 healthy subjects were enrolled in this study for measurement of serum concentrations of hs-CRP, TC and HDL-C.The concentration of hs-CRP and TC/HDL-C ratio was significantly higher in CHD patients than in the control subjects (P0.01). The positivity rate by detecting both the two markers (0.950) was higher than that of single marker detection of either hs-CRP (0.850) or TC/HDL-C (vs 0.767).Detection of hs-CRP combined with determination of TC/HDL-C may facilitate early diagnosis of CHD.

To study the changes in plasma adrenomedullin (ADM) and proadrenomedullin N-terminal 20 peptide (PAMP) concentrations and their clinical significance in the pathological process of congestive heart failure (CHF).Plasma ADM and PAMP concentrations in 45 patients with CHF (according to the functional classification of New York Heart Association, NYHA) and 20 control subjects were measured by specific radioimmunoassay.Plasma ADM concentrations were 51.464+/-.52 pg/ml and 70.39+/-3.22 pg/ml respectively in patients of NYHA class II and class III, which were significantly higher than those in control subjects (24.12+/-1.59 pg/ml, P0.05 for both comparisons), while significant differences in plasma PAMP concentrations were not identified in the 2 groups of patients (6.24+/-1.71 pg/ml and 7.38+/-1.28 pg/ml, respectively) in comparison with the control level(8.56+/-2.44 pg/ml, P0.05 for both comparisons). Patients of NYHA class IV, when compared with the 2 groups of patients mentioned above, had significantly decreased plasma ADM and PAMP concentrations (36.33+/-2.17 pg/ml and 2.79+/-0.89 pg/ml respectively, P0.05 in both cases), but had higher plasma ADM and lower PAMP concentrations when compared with the control subjects, (P0.05 respectively).The changes of plasma ADM and PAMP concentrations at different stages of CHF indicate intramolecular regulation disturbances of vasodilator peptides of proadrenomedullin, and ADM may play a more important role in the development of CHF.

To investigate the changes in plasma levels of adrenomedullin (ADM) and cyclic adenosine monophosphate (cAMP) in patients with chronic heart failure (CHF) in an attempt to understand the role of ADM in the occurrence and development of CHF.The plasma levels of cAMP and ADM were measured by radioimmunoassay in 45 patients with CHF (including 10 of NYHA classII, 15 of class III, and 20 of class IV) and 20 healthy controls respectively.Plasma ADM and cAMP levels significantly increased in patients of NYHA class II, III, and IV as compared with the healthy controls (P0.05), with those of class III patients being the highest. Positive correlation between ADM and cAMP was noted in CHF patients(r=0.735, P0.01).Plasma levels of ADM and cAMP were in close correlation with the degree of heart failure, varying dynamically with the development of heart failure. There was mutual accommodation between ADM and cAMP, and increased cAMP level partly results from elevated ADM level in CHF patients.