ABSTRACT
Objective: To explore the relationship between prevalence of atrial fibrillation (AF), iskhemia stoke and CHA2DS2-VASc score in patients≥65 years in order to provide prevention and treatment basis in clinical practice. Methods: A total of 5016 patients admitted in our hospital from 2013-10 to 2015-10 were enrolled. The patients were divided into 2 groups: AF group, n=437 and Non-AF patients, n=4579; according to age, the patients were further assigned into 4 subgroups as <65 years subgroup, (65-74) years subgroup, (75-84) years subgroup and ≥85 years subgroup. The risk factors for AF occurrence were retrospectively studied. Results: Compared with the Non-AF group, the patients in AF group had the elder age and more male gender, both P<0.001; more patients combining with hypertension, coronary artery disease (CAD), diabetes, sick sinus syndrome and rheumatic heart disease, all P<0.001. Age, male gender, CAD, sick sinus syndrome and rheumatic heart disease were the independent risk factors for AF occurrence. Compared with Non-AF group, AF group showed the higher prevalence rate of ischemic stroke and the elder onset age, both P<0.01. For non-valvular AF, the ratio of patients with CHA2DS2-VASc score≥2 was higher than those with CHA2DS2-VASc score<2 and the rate of anticoagulant therapy was decreasing by age increasing, all P<0.001. Conclusion: Age, male gender, CAD, sick sinus syndrome and rheumatic heart disease were independently related to AF occurrence. Non-valvular AF patients had the higher risk for ischemic stroke than non-AF patients, anticoagulation therapy should be conducted at the early stage.
ABSTRACT
Objective: To explore the relationship between serum level of high-sensitivity cardiac troponin T (hs-cTnT) and atrial ifbrillation (AF) occurrence in patients with stable coronary artery disease (CAD). Methods: A total of 1011 patients with stable CAD treated in our hospital from 2013-01 to 2015-09 were retrospectively studied. According to quartiles of hs-cTnT, the patients were divided into 4 groups: Group① the patients with hs-cTnT≤7ng/L, n=283, Group② hs-cTnT 7-10ng/L,n=238, Group③ hs-cTnT 10-15ng/L,n=272 and Group④ hs-cTnT>15ng/L,n=218. The relationship between hs-cTnT level and AF occurrence rate was studied; the risk factors for AF occurrence were explored by multi stepwise Logistic regression analysis. Results: There were 127/1011 (12.6%) patients combining AF and 884 (87.4%) with simple type stable CAD. AF patients had the higher serum level of hs-cTnT than non-AF patients 17.0 (12.0, 25.0) ng/L vs 10.0 (7.0, 13.0) ng/L,P Conclusion: Increased serum level of hs-cTnT was closely related to AF occurrence in patients with stable CAD.
ABSTRACT
Objective: To explore the relationship between lower extremity atherosclerosis disease (LEAD) and cardiovascular risk factors in elder people. Methods: A total of 700 consecutive patients receive lower extremity Color Doppler ultrasound in our hospital from 2013-05 to 2014-11 were investigated. The patients were divided into 3 age groups: Young and middle group, n=83, Elder group, n=377 and Senile group, n=240. Based on ultrasound scoring system, the patients were divided into 4 groups: Normal group, n=112, Mild atherosclerosis (Mild) group, n=81, Moderate group, n=466 and Severe group, n=41. The cardiovascular risk factors among different groups were compared. Results: Multivariate unconditional logistic regression analysis showed that age, smoking, history of diabetes, uric acid (UA), ankle-brachial index (ABI) were the independent risk factors for LEAD (B=0.144, 1.496, 0.963, 0.004, -2.510; 95% CI: 1.120-1.190, 2.257-8.824, 1.456-4.716, 1.001-1.007, 0.012-0.534;P=0.000, 0.000, 0.001, 0.006, 0.009 respectively. Ordinal logistic regression analysis indicated that age, male gender, smoking, ABI, UA, history of hypertension were related to the severity of atherosclerosis (B=0.130, 0.737, 0.592, -3.365, 0.003, 0.735; 95% CI: 0.097-0.162, 0.222-1.252, 0.052-1.132, -4.674 to -2.055, 0.001-0.005, 0.313-1.157;P=0.000, 0.005, 0.032, 0.000, 0.005, 0.001 respectively. Compared with Young and Middle groups, Elder and Senile groups had increased rates of moderate and severe arteriosclerotic lesions; compared with Elder group, Senile group presented the higher incidence of moderate and severe lesions, allP Conclusion: Lower extremity atherosclerosis lesions were more severe in elder patient, and it was particularly severe in senile patients.
ABSTRACT
Objective The aim of our study was to investigate the effects and mechanisms of ghrelin on neovascularization in atherosclerosis plaque. Methods 30 male New Zealand rabbits were randomly divided into normal control group ( CON group) , atherosclerosis model group ( AS group) , and ghrelin treatment group ( ghrelin group) , and each group of 10 rabbits. The AS group and ghrelin group underwent balloon-induced arterial wall injury and then fed with high fat diet, the CON group was fed only on a regular diet. They were all fed for 3 months. Then the ghrelin group was given ghrelin 25μg·kg-1 ·d-1 , the other two groups received the same amount of sterile normal saline only. Four weeks later, body weight and blood lipids were detected. The thickness ratio of the intima to media was measured by HE staining. Degree of intra-plaque angiogenesis was evaluated by CD31+ cells immunohisto-chemistry. The vascular endothelial growth factor ( VEGF ) and vascular endothelial growth factor receptor 2 ( VEGFR2) were detected by quantitative realtime PCR and Western blot. The expressions of matrix metalloproteinase ( MMP)-2 and MMP-9 were detected by immunohistochemistry and Western blot. Results ( 1 ) No significant differences in body weight and blood lipids were found between the AS group and the ghrelin group(P>0. 05), but both items were significantly higher than those of the CON group(P<0. 05). (2)The thickness ratio of the intima to media in the ghrelin treated group was distinctly less than that in the AS group(P<0. 05). (3)Compared with the AS group, the ghrelin group showed significantly decreased microvascular density and the expressions of VEGF and VEGFR2 (P<0. 05). (4)Compared with the AS group, ghrelin dramatically inhibited the plaque contents of MMP-2 and MMP-9 ( P<0. 05 ). Conclusions Ghrelin is able to inhibit the growth of neovascularizationin in the atherosclerotic plaque and the development of plaque. And these beneficial effects derive from downregulation of VEGF, VEGFR2, MMP-2, and MMP-9 at the advanced stage of atherosclerosis in rabbits.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects and related mechanisms of ghrelin on myocardial neovascularization in diabetic rats with experimental myocardial infarction (MI).</p><p><b>METHODS</b>Adult male SD rats were divided into six groups (n = 20 each group): control, diabetes mellitus (DM), MI, DM+MI, DM+MI+ghrelin, DM+MI+ghrelin+D-Lys3-GHRP-6 (GHSR1a inhibitor). DM was induced by streptozotocin (STZ, 60 mg/kg), 3 months later, MI was induced by left anterior descending artery ligation in DM rats. DM+MI+ghrelin group received ghrelin 200 µg×kg(-1)×d(-1) and DM+MI+ghrelin+D-Lys3-GHRP-6 group received ghrelin 200 µg×kg(-1)×d(-1) and D-Lys3-GHRP-6 50 mg×kg(-1)×d(-1) for 4 weeks. Then, cardiac function was measured by echocardiography, microvascular density (MVD) was measured by CD34 immunohistochemistry, myocardial infarct size was determined by Masson staining, the mRNA and protein expressions of vascular endothelial growth factor (VEGF) and receptors Flk-1, Flt-1 were detected by real-time PCR and Western-blot, respectively.</p><p><b>RESULTS</b>Compared with MI group, MVD (15.3 ± 1.0 vs.20.7 ± 1.6, P < 0.05), left ventricular ejection fraction (LVEF) ((64.2 ± 3.4)% vs. (81.3 ± 3.8)%, P < 0.01), left ventricular fractional shortening (LVFS) ((31.7 ± 1.1)% vs. (48.8 ± 3.3)%, P < 0.01) and the mRNA and protein expression of VEGF, Flk-1 and Flt-1 (P < 0.01) were reduced, while myocardial infarct size ((55.8 ± 3.1)% vs. (35.7 ± 2.5)%, P < 0.01) was increased in DM+MI group. These effects were partly reversed in DM+MI+ghrelin group and the beneficial effects of ghrelin were partly abolished by D-Lys3-GHRP-6 (all P < 0.05).</p><p><b>CONCLUSIONS</b>Our results demonstrate that ghrelin could improve microvascular density, cardiac function, and reduce myocardial infarct size of diabetic rats with myocardial infarction via modulating GHSR1a-mediated expressions of VEGF, Flk-1 and Flt-1.</p>
Subject(s)
Animals , Male , Rats , Blotting, Western , Coronary Vessels , Diabetes Mellitus, Experimental , Echocardiography , Ghrelin , Physiology , Myocardial Infarction , Myocardium , Neovascularization, Physiologic , Oligopeptides , Vascular Endothelial Growth Factor A , Ventricular Function, LeftABSTRACT
Objective To explore the effects of transplantated bone marrow mesenchymal stem cells (MSCs) on myocardial fibrosis with the aid of ultrasound-mediated microbubbles (MB) and bispecific antibody(BiAb) combination.Methods With the aid of MB,isolated MSCs from male mice and the BiAb were transfused into female mice with isoproterenol-induced myocardial fibrosis via tail vein (MSCs + BiAb + MB group).BiAb was producted with anti-CD29 which can recognize MSCs and anti-myosin light chain antibody (AMLCA) which can specifically bind to injured myocardium.There were six groups investigated:MSC + BiAb + MB,MSC,BiAb,MB,MSC + BiAb,untreated,and control groups.Five weeks after treatment administration,the expressions of sex-determining region of Y-chromosome (SRY) in myocardium were detected by fluorescent quantitative PCR.The distribution of collagen was observed by sirius red staining.Heat shock protein-70 (HSP-70) in myocardium was detected by immunohistochemistry.Results The highest homing number of MSCs was in the MSCs + BiAb + MB group,MSCs + BiAb group ranked the second,and lowest in MSCs group.Compared to the untreated group,the MSCs + BiAb + MB,MSCs + BiAb and MSCs groups had less collagen deposition (P ＜0.05),and decreased level of HSP-70.Compared to those of the MSCs group,the collagen deposition were decreased in MSCs + BiAb + MB group (P ＜0.05).Conclusions MB and BiAb can promote the homing number of MSCs in mice.MB can further the homing rate and the repairing efficacy of MSCs.The homing MSCs can prevent the process of myocardial fibrosis.And HSP-70 was involved in the internal mechanism.
ABSTRACT
BACKGROUND: Most of hematopoietic growth factor regulates proliferation and differentiation of blood cells through JAKs-STATs signal transduction pathway. Total saponins of Panax ginseng (TSPG) can promote in vitro differentiation of CD34+ hematopoietic progenitor cells into erythroid cells, with similar effectiveness of hematopoietic growth factor.Erythropoietin receptor (EpoR) expression on the cell membrane of progenitor cells is critical during the erythroid differentiation process.OBJECTIVE: To investigate the molecular mechanism of TSPG to induce erythroid cells through erythropoiesis and its receptor-mediated JAK2/STAT5 signal transduction.DESIGN, TIME AND SETTING: An in vitro cytological observation. The study was performed at the Department of Histology and Embryology, Institute of Basic Medicine, Chongqing Medical University from May 2006 to October 2008.MATERIALS: Umbilical cord blood of normal full-term pregnancy was provided by the First Hospital of Chongqing Medical University. TSPG, purity＞95%, provided by Chongqing Institute of Traditional Chinese Medicine, was diluted in RPMI-1640 for work concentration of 1 g/L and degermed by positive pressure filtration.in RPMI-1640 culture solution containing horse serum, with various dilutions of TSPG (0 as blank control, 10, 25, 50, 75,100 mg/L). The MNCs were cultured on 96-well culture plate, with 0.2 mL in each well. Early erythroid cells were counted on were harvested and cultured separately in RPMI-1640 culture solution containing 10% horse serum as control group and in TSPG (25 mg/L)- conditioned culture system as experimental group. 5 U/mL Epo was added for 0, 2, 5 and 30 minutes.Immunoprecipitation of JAK2/STAT5 was used for the effect of TSPG on Epo/EpoR-induced tyrosine phosphorylation of JAK2/STAT5.MAIN OUTCOME MEASURES: Effect of TSPG on proliferation of erythroid progenitor cells from human umbilical cord blood;Effect of Epo on the proliferation of hematopoietic cells; Effect of TSPG on EpoR expression of the umbilical blood cells; tyrosine phosphorylations of JAK2 and STAT5.RERULTS: TSPG (10-75 mg/L) promoted the colony formation of BEU-E, CFU-E, and the preferential differentiation into erythroid lineage cells was most induced from 25 mg/L of TSPG. Using the colorimetric MTT assay, MNCs exhibited proliferative responses to Epo (2-50 U/mL) reaching maximum at 5 U/mL Epo. The addition of TSPG did not increase the expression of EpoR after MNCs were incubated in the presence of with or without TSPG for 24 hours. The pretreatment with TSPG for 24 hours enhanced Epo-induced tyrosine phosphorylation of JAK2 and STAT5 (STAT5a and STAT5b).