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Objective: To investigate the risk factors of moderate or severe perivalvular leakage (PVL) after transcatheter aortic valve replacement (TAVR) with Veneus-A valve. Methods: This study was a single-center case-control study. The clinical data of patients with severe aortic stenosis, who underwent TAVR in the Department of Cardiology of Second Affiliated Hospital of Army Medical University from October 2017 to January 2021, were analyzed. According to the circumferential extent of prosthetic valve paravalvular regurgitation measured by transthoracic echocardiography before discharge (patients who died in hospital were referred to transesophageal echocardiography results after valve implanted), the patients were divided into moderate or severe PVL group and mild or non-PVL group. The clinical features, CT scan and analysis results of aortic root were compared between the two groups. Multivariate logistic regression analysis was used to identify the independent risk factors of postoperative moderate or severe PVL, and receiver operating characteristic (ROC) curve was used to explore the predictive value of related factors. Results: Eighty-two patients (mean age: (70.9±6.5) years, 46 males) were included in the analysis, there were 16 patients in the moderate or severe PVL group and 66 patients in the mild or non-PVL group. The proportion of male gender, depth of valve implantation, size of valve annulus and left ventricular outflow tract (LVOT), and coverage index of LVOT were significantly higher in moderate or severe PVL group than those in mild or non-PVL group (Pall<0.05). As there was a strong collinearity among the valve annular short diameter, LVOT short diameter and LVOT coverage index (partial correlation coefficient R 0.251-0.779, P<0.05), these parameters were not entered in regression model. Multivariate logistic regression analysis showed that valve implantation depth(OR=1.239,95%CI 1.036-1.442,P=0.023), aortic angulation(OR=1.128, 95%CI 1.044-1.312,P=0.038)and LVOT tract coverage index (OR=1.123, 95%CI1.003-1.315, P=0.032) were independent risk factors for moderate or severe PVL after TAVR. The ROC curve showed that the valve implantation depth could predict the occurrence of moderate or severe PVL after TAVR (area under ROC curve (AUC)=0.697, 95%CI 0.554-0.851, P=0.039). Conclusion: Among patients with severe aortic stenosis who undergo TAVR with Venus-A valve, the implantation depth, aortic angulation and LVOT coverage index are independent risk factors of moderate/severe PVL after TAVR, among which valve implantation depth could be used to predict the occurrence of moderate/severe PVL after TAVR.
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<p><b>OBJECTIVE</b>To study the effects of carvedilol combined with perindopril on Ca(2+) pump activity and the density of Ca(2+)-release channel ryanodine receptor (RyR2) in the myocardial sarcoplasmic reticulum (SR) in rats with chronic heart failure caused by myocardial infarction.</p><p><b>METHODS</b>Rat models of chronic heart failure established by left coronary artery ligation were divided into different groups and treated with carvedilol (6 mg.kg(-1).d(-1)), perindopril (4 mg.kg(-1).d(-1)), terazosin (2 mg.kg(-1).d(-1)), or the combination of carvedilol (6 mg.kg(-1).d(-1)) and perindopril (4 mg.kg(-1).d(-1)) for 9 weeks. Another 12 rats with sham operation served as the sham-operated group. The hemodynamic parameters, activity of SR Ca(2+) pump, and RyR2 density were determined.</p><p><b>RESULTS</b>Compared with shame-operated group, the rats with chronic heart failure showed significantly increased left ventricular end-diastolic pressure (LVEDP) (P<0.01) and decreased +dP/dtmax, -dp/dtmax, activity of SR Ca(2+) pump and density of RyR2 (P<0.01). Both monotherapies with carvedilol and perindopril attenuated the increment of LVEDP, and significantly increased +dp/dtmax, -dp/dtmax, activity of SR Ca(2+) pump and density of RyR2 (P<0.01). Combined treatment even further enhanced the therapeutic effects, whereas terazosin produced no obvious effect. The activity of SR Ca(2+) pump was strongly correlated to +dp/dtmax and -dp/dtmax (r=0.596 and 0.684, respectively, P<0.01).</p><p><b>CONCLUSION</b>Prolonged treatment with beta-blocker carvedilol in combination with ACE inhibitor perindopril may improve the hemodynamic parameters, enhance Ca(2+) pump activity and increase the density of RyR2 of myocardial SR more effectively than either monotherapy in preventing and treating chronic heart failure following myocardial infarction.</p>
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Animais , Masculino , Ratos , Cálcio , Metabolismo , Carbazóis , Farmacologia , Usos Terapêuticos , Quimioterapia Combinada , Insuficiência Cardíaca , Tratamento Farmacológico , Metabolismo , Infarto do Miocárdio , Metabolismo , Perindopril , Farmacologia , Usos Terapêuticos , Propanolaminas , Farmacologia , Usos Terapêuticos , Ratos Wistar , Canal de Liberação de Cálcio do Receptor de Rianodina , Retículo Sarcoplasmático , MetabolismoRESUMO
<p><b>OBJECTIVE</b>To explore the underlying mechanism of mesenchymal stem cells (MSCs) transfer induced cardiac function improvement in failing hearts.</p><p><b>METHODS</b>Congestive heart failure (CHF) was induced in rats by cauterization of the heart wall. MSCs were cultured from autologous bone marrow and injected into the border zone and the remote myocardium 5 days after cauterization.</p><p><b>RESULTS</b>Ten weeks later, cardiomyocyte nucleus mitotic index, capillary density and expression of insulin-like growth factor 1 (IGF-1), hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) were significantly increased in the border zone and significantly reduced in the remote myocardium in CHF rats (all P<0.05 vs. sham). Besides cardiac function improvement and left ventricular remodeling attenuation evidenced by hemodynamic and echocardiographic examinations, expressions of IGF-1, HGF and VEGF in the remote myocardium and in the border zone were also significantly upregulated (P<0.05 or P<0.01 vs. CHF), and cardiomyocyte nucleus mitotic index as well as capillary density were significantly increased in CHF rats with MSCs (P<0.05 or P<0.01 vs. CHF). Moreover, collagen area was significantly reduced and myocardial area was significantly increased in the border zone in these rats too.</p><p><b>CONCLUSION</b>Autologous MSC implantation upregulated expressions of growth factors enhanced cardioangiogenesis which might be the underlying mechanisms for improved cardiac function and attenuated left ventricular remodeling induced by MSCs transplantation in failing rat myocardium.</p>
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Animais , Masculino , Ratos , Modelos Animais de Doenças , Insuficiência Cardíaca , Metabolismo , Terapêutica , Fator de Crescimento de Hepatócito , Metabolismo , Fator de Crescimento Insulin-Like I , Metabolismo , Transplante de Células-Tronco Mesenquimais , Miocárdio , Metabolismo , Ratos Sprague-Dawley , Transplante Autólogo , Fator A de Crescimento do Endotélio Vascular , Metabolismo , Remodelação VentricularRESUMO
<p><b>OBJECTIVE</b>To observe the effects of C reactive protein (CRP) on endothelial progenitor cell (EPCs) function.</p><p><b>METHODS</b>Mononuclear cells (MNCs), isolated from bone marrow by density gradient centrifugation combined with adherent cell filtration, were plated on fibronectin coated culture dishes. After 7 days, adherent cells were cultured with different concentrations of CRP (0, 5, 10, 15, 20 microg/ml) for 48 hours. EPCs proliferation and migration ability were observed and adhesion assay was performed. The eNOS mRNA expression of EPCs were measured by RT-PCR.</p><p><b>RESULTS</b>The number of EPCs in CRP groups (10, 15, 20microg/ml) was obviously lower than that in control group (54 +/- 3, 47 +/- 3, 39 +/- 5 vs.60 +/- 3, P < 0.01). EPCs proliferation capacity was inhibited in CRP groups (10, 15, 20 microg/ml) compared with that in control group (0.297 +/- 0.036, 0.273 +/- 0.013, 0.259 +/- 0.035 vs. 0.345 +/- 0.014, P < 0.01). EPCs migration capacity was inhibited significantly in CRP groups (5, 10, 15, 20 microg/ml) than that in control group (28 +/- 2, 22 +/- 3, 19 +/- 3, 16 +/- 2 vs. 30 +/- 2, P < 0.05). EPCs adhensive number was lower in CRP groups than that in control group (11 +/- 2, 9 +/- 2, 6 +/- 2, 5 +/- 1 vs. 12 +/- 2, P < 0.05). The mRNA expressions of eNOS in CRP groups were significantly lower in control group. And compared with control group, NOS activity decreased significantly in CRP groups (10, 15, 20 microg/ml) (57.44 +/- 3.25, 48.37 +/- 3.86, 36.82 +/- 4.89 vs. 68.56 +/- 2.82, P < 0.01).</p><p><b>CONCLUSION</b>CRP could both reduce EPCs number and inhibit EPCs functions.</p>
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Animais , Masculino , Ratos , Células da Medula Óssea , Biologia Celular , Proteína C-Reativa , Farmacologia , Células Cultivadas , Células Endoteliais , Metabolismo , Óxido Nítrico Sintase Tipo III , Metabolismo , Ratos Sprague-Dawley , Células-Tronco , Biologia CelularRESUMO
<p><b>OBJECTIVE</b>To develop a method to obtain and identify human coronary artery endothelial cells obtained during percutaneous coronary interventions (PCI).</p><p><b>METHODS</b>Coronary guide wires were used to obtain endothelial cells from coronary arteries in 28 patients undergoing PCI. The cells were eluted from the wire tips and then purified by magnetic beads coated with anti-CD146 antibody. von Willebrand factor (vWF) was used as an immunocytochemical marker for endothelial cells. The cellular viability was evaluated by observing cell membrane integrity and energy-dependent uptake of DiI-labeled acetylated low-density lipoprotein.</p><p><b>RESULTS</b>An average of 96 coronary artery endothelial cells with good viability per patient were obtained by one guide wire. vWF identification showed their endothelial morphology and immunoreactivity.</p><p><b>CONCLUSION</b>The viable coronary endothelial cells could be obtained during routine percutaneous coronary interventions combined with magnetic beads isolation technique. These cells may be used for further cellular functional analyses (such as immunocytochemistry and molecular biology) and expand our understanding on mechanisms of coronary artery diseases.</p>
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Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Biópsia , Métodos , Vasos Coronários , Biologia Celular , Patologia , Endotélio Vascular , Biologia Celular , PatologiaRESUMO
Background Stromal cell-derived factor-1_?(SDF-1_?)has been demonstrated to be essential for stern cell mobilization/homing.Recent evidence indicates that SDF-1_? has been expressed in injured carotid arter- ies.Besides,high SDF-1_? plasma levels are clinically associated with stable coronary artery disease.Objective To investigate whether SDF 1 involves in mobilization of endothelial progenitor cells(EPC)and reendothelialization after vascular injury.Methods SDF-1_? was detected by RT-PCR and Western blot in carotid arteries of mice at different time points after wire-induced injury.SDF-1_? determination in peripheral blood samples and BM was per- formed by SDF-1_? enzyme-linked immunosorbent assay(ELISA)kit.EPC in peripheral blood collected at different time points after vascular injury were quantified by flow cytornetry.In subgroup,blocking SDF-1 rnonoclonal anti- body was injected,peripheral blood EPC were quantified after vascular injury and reendothelialization of injured ar- teries was determined 14 days later.Results Expression of SDF-1_? was evident at day 1,and peaked at day 3 after arterial injury.A rise in plasmatic concentration of SDF-1_? and a significant reduction of SDF-1_? in bone marrow concentration was noticed at all time points following injury.The amount of circulating EPC was increased shortly after induction of vascular injury and persisted up to 7 days(P