ORCID Profile
0000-0001-6523-7488
Current Organisations
The General Hospital of Shenyang Military
,
PLA Heart Blood Vessel Internal Surgery Research Institute The General Hospital of ShenYang Military Command
,
Key Laboratory of Regenerative Medicine of Liaoning
,
Key Laboratory of Military
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Publisher: Elsevier BV
Date: 02-2017
DOI: 10.1016/J.AMJCARD.2016.10.017
Abstract: Oxidative stress has been considered to be an important factor contributing to postoperative atrial fibrillation (PoAF). Mitochondrial DNA (mtDNA) copy number in peripheral blood has been found to be associated with a patient's oxidative stress. Therefore, we sought to determine whether there was association between mtDNA copy number and the onset of atrial fibrillation. mtDNA copy numbers were measured using the quantitative real-time polymerase chain reaction in peripheral blood from 485 consecutive patients with sinus rhythm undergoing coronary artery bypass grafting. The blood was collected before surgery. In the cohort, the incidence of PoAF was 20.8% (101/485). The mean mtDNA copy number was significantly higher in patents with PoAF than in those with sinus rhythm (36.43 vs 16.63, p <0.001). The receiver operating characteristic analysis proved that the mtDNA copy number could predict PoAF with good sensitivity and specificity (area under the curve = 0.814, cutoff = 20.91, sensitivity = 70.3%, specificity = 80.2%, p <0.001). On multivariate logistic and Cox regression analysis, mtDNA copy number was shown to be a significant independent risk factor for PoAF (odds ratio = 10.01, p <0.001 and hazard ratio = 7.011, p = 0.004). There was a strong positive correlation between mtDNA copy number and malondialdehyde in patients with PoAF (r = 0.449, p = 0.01). In conclusion, we showed that elevated mtDNA copy number in peripheral blood is associated with PoAF. Further investigation is needed to validate mtDNA copy number as a predictive biomarker for PoAF and to explore its potential role in arrhythmogenesis.
Publisher: Springer Science and Business Media LLC
Date: 24-08-2014
DOI: 10.1007/S12013-014-0186-Z
Abstract: Patients with rheumatic heart disease (RHD) often experience persistent atrial fibrillation (AF) associated with adverse atrial structural remodeling (ASR) manifested by atrial fibrosis and left atrial enlargement. The aim of this study was to explore the potential molecular signaling mechanisms for atrial fibrosis and ASR. Twenty RHD patients with persistent AF and 10 RHD patients with sinus rhythm (Group A) were recruited in our study, which all underwent transthoracic echocardiography. Right atrial appendage (RAA) tissue s les were obtained from these patients during mitral/aortic valve replacement operation. The AF patients were further ided into two groups according to left atrial diameter (LAD): Group B with LAD ranging 50-65 mm and Group C with LAD >65 mm. Histological examinations were performed with hematoxylin-eosin staining and Masson's trichrome staining. Atrial angiotensin II (AngII) content was measured by ELISA. Rac1 and STAT3 protein levels were determined by Western blot analysis. Hematoxylin-eosin staining demonstrated highly organized arrangement of atrial muscles in control Group A and significant derangement in both Group B and C AF patients with reduced cell density and increased cell size. Moreover, Masson's trichrome staining showed that atrial myocytes were surrounded by large trunks of collagen fibers in both Group B and C, but not in Group A. There was a positive correlation between atrial tissue fibrosis and LAD. AngII content was markedly higher in Group C than in Group B than in Group A, which was positively correlated with LAD. Similarly, Rac1 and STAT3 protein levels were found considerably higher in Group C and B than in Group A with excellent correlation to LAD. Our study unraveled for the first time the AngII/Rac1/STAT3 signaling as a mechanism for ASR thereby AF in a particular clinical setting-RHD patients with persistent AF and indicated inhibition of this pathway may help ameliorating adverse ASR.
Publisher: Elsevier BV
Date: 04-2018
DOI: 10.1016/J.HLC.2017.04.005
Abstract: Coronary artery bypass graft surgery (CABG) with mitral valve surgery is undisputed in severe ischaemic mitral regurgitation (IMR) treatment, but the controversy is whether mitral valve replacement (MVR) or mitral valvuloplasty (MVP) should be used. Data was collected from 130 cases of severe IMR patients who underwent CABG and MVP or MVR from June 2010 to June 2015 to compare the short-term efficacy of CABG with MVP or MVR in the treatment of severe IMR patients. There were 70 cases in the MVP group and 60 in the MVP group. The postoperative major cardiac cerebral vascular events and left ventricular ejection fraction (LVEF), left ventricular end-systolic diameter (LVESD), and left ventricular end-diastolic diameter (LVEDD) were recorded. Eleven patients died in hospital, the remaining patients were followed up for 12 months 18 patients died. The cumulative survival rate and the major cardiac cerebrovascular events were not significantly different. There was no significant change in LVEF, but LVEDD, LVESD and systolic pulmonary artery pressure (sPAP) improved significantly, and there was no difference between the groups. In the MVR group, the rate of postoperative moderate or severe mitral regurgitation patients was significantly less than that in the MVP group. The short-term survival rate, reversal of left ventricular remodelling and major cardiac or cerebrovascular events post-CABG combined with MVP were not significantly different to those with CABG combined with MVR in the treatment of severe IMR, but long-term efficacy remains to be observed.
Publisher: Springer Science and Business Media LLC
Date: 11-05-2010
DOI: 10.1007/S10456-010-9169-X
Abstract: Sendai viral vector (SeV) is emerging as a promising vector for gene therapy. However, little information is available regarding the combination of SeV-mediated gene and mesenchymal stem cell (MSC) therapy in dealing with ischemic diseases. In this study, we infected SeV to the MSCs in vitro and injected MSCs modified with SeV harboring human angiopoietin-1 gene (SeVhAng-1) into the ischemic limb of rats in vivo. We found SeV had high transductive efficiency to the MSCs. Both MSCs and SeVhAng-1-modified MSCs improved the blood flow recovery and increased the capillary density of the ischemic limb, compared with the control. However, in contrast to MSCs, SeVhAng-1-modified MSCs had a better improvement of blood flow recovery in the ischemic limb. We further found the ischemic limb injected with SeVhAng-1-modified MSCs had strong expression of p-Akt, which improved survival of MSCs injected into the ischemic limb. This indicated SeVhAng-1 modification enhanced angiogenetic effect of MSCs by both angiogenesis and cell protection. We conclude that SeVhAng-1-modified MSCs may serve as a more effective tool in dealing with ischemic limb disease.
Publisher: Hindawi Limited
Date: 2016
DOI: 10.1155/2016/4967275
Abstract: Objective . To investigate the effects of diabetes mellitus (DM) in patients undergoing off-pump coronary artery bypass grafting (OPCAB). Method . A total of 728 patients with DM and 1380 patients without DM who underwent OPCAB treatment from March 2012 to April 2015 were reviewed. The effects of DM on intraoperative variables and postoperative complications were determined using propensity score analysis. Results . Two well-matched subgroups were selected using propensity score analysis (DM = 728, no-DM = 728) to compare the perioperative outcome. The duration of the ICU stay, in hours (55.2 ± 53.0 versus 49.29 ± 51.30, P 0.05 ), postoperative new-onset atrial fibrillation (20.9% versus 14.97%, P 0.05 ), and postoperative infection (9.2% versus 4.67%, P 0.05 ) were greater in DM patients, as indicated by univariate analysis. Conclusion . OPCAB was found to be effective in DM patients, but postoperative infection and postoperative new-onset atrial fibrillation were found to be more likely to occur in DM patients than in other patients. DM was found to be a powerful risk factor for postoperative infection and postoperative new-onset atrial fibrillation.
Publisher: Elsevier BV
Date: 09-2013
DOI: 10.1016/J.GENE.2013.05.002
Abstract: Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the major enzymes responsible for alcohol metabolism in humans. Emerging evidences have shown that functional polymorphisms in ADH and ALDH genes might play a critical role in increasing coronary artery disease (CAD) and myocardial infarction (MI) risks however, in idually published studies showed inconclusive results. The aim of this meta-analysis is to evaluate the associations between the genetic polymorphisms of ADH and ALDH genes with susceptibility to CAD and MI. A literature search was conducted on PubMed, Embase, Web of Science and Chinese BioMedical databases from inception through December 1st, 2012. Crude relative risks (RRs) with 95% confidence intervals (CIs) were calculated. Twelve case-control studies were included with a total of 9616 subjects, including 2053 CAD patients, 1436 MI patients, and 6127 healthy controls. Meta-analysis showed that mutant genotypes (GA+AA) of the rs671 polymorphism in the ALDH2 gene were associated with increased risk of both CAD and MI (CAD: RR=1.20, 95%CI: 1.03-1.40, P=0.021 MI: RR=1.32, 95%CI: 1.11-1.57, P=0.002). However, there were no significant associations of ADH genetic polymorphisms to CAD and MI risks (CAD: RR=0.92, 95%CI: 0.73-1.15, P=0.445 MI: RR=0.93, 95%CI: 0.84-1.03, P=0.148). In conclusion, this meta-analysis provides strong evidence that ALDH2 rs671 polymorphism may be associated with increased risks of CAD and MI. However, further studies are still needed to accurately determine whether ADH genetic polymorphisms are associated with susceptibility to CAD and MI.
Publisher: Springer Science and Business Media LLC
Date: 30-05-2017
Publisher: Genetics and Molecular Research
Date: 2015
Publisher: Oxford University Press (OUP)
Date: 15-12-2010
DOI: 10.1016/J.EJCTS.2010.10.041
Abstract: The goal of our study was to report our experience of using half rotation of the truncus arteriosus plus arterial switch, as a modification of the Nikaidoh procedure, for anatomic repair of transposition of the great arteries (TGA) with ventricular septal defect (VSD) and pulmonary outflow tract obstruction (pulmonary stenosis (PS)). From December 2006 to December 2009, 11 patients (six male, five female) underwent half rotation of the truncus arteriosus plus arterial switch for repair of TGA, VSD, and PS or double-outlet right ventricle (DORV) at our heart center. There was no operative death. All patients had relief of left ventricular outflow tract obstruction (LVOTO) as determined by direct pressure measurements intraoperatively. Echocardiography was performed for all patients intraoperatively and before discharge. Two patients had mild aortic regurgitation and two patients had mild pulmonary regurgitation. For a median follow-up of 15 months (range 6-42 months), all patients were alive. Echocardiography was performed at 3, 6, 12, 24 and 36 postoperative months. All patients have normal ventricular function. No evidence of LVOTO was founded in all patients. Two patients had mild aortic regurgitation and three patients had mild to medium pulmonary regurgitation. Half rotation of the truncus arteriosus plus arterial switch, as a modification of the Nikaidoh procedure, is a good alternative treatment for complete anatomic repair for TGA, VSD, and PS or DORV with malposition of great arteries and PS. The technique might allow to reconstruct biventricular outflow tract, preserve competence and growth potential of the pulmonary root with valves and decrease the probability of reoperation. Its long-term benefits need to be evaluated with a large number of patients and longer follow-up.
Publisher: Elsevier BV
Date: 02-2018
DOI: 10.1016/J.BBADIS.2017.11.023
Abstract: It has been demonstrated that the anti-oxidative and cardioprotective effects of melatonin are, at least in part, mediated by its membrane receptors. However, the direct downstream signaling remains unknown. We previously found that melatonin ameliorated myocardial ischemia-reperfusion (MI/R) injury in diabetic animals, although the underlying mechanisms are also incompletely understood. This study was designed to determine the role of melatonin membrane receptors in melatonin's cardioprotective actions against diabetic MI/R injury with a focus on cGMP and its downstream effector PKG. Streptozotocin-induced diabetic Sprague-Dawley rats and high-glucose medium-incubated H9c2 cardiomyoblasts were utilized to determine the effects of melatonin against MI/R injury. Melatonin treatment preserved cardiac function and reduced oxidative damage and apoptosis. Additionally, melatonin increased intracellular cGMP level, PKGIα expression, p-VASP/VASP ratio and further modulated myocardial Nrf-2-HO-1 and MAPK signaling. However, these effects were blunted by KT5823 (a selective inhibitor of PKG) or PKGIα siRNA except that intracellular cGMP level did not changed significantly. Additionally, our in vitro study showed that luzindole (a nonselective melatonin membrane receptor antagonist) or 4P-PDOT (a selective MT
Publisher: Springer Science and Business Media LLC
Date: 09-07-2013
Publisher: S. Karger AG
Date: 06-12-2014
DOI: 10.1159/000369381
Abstract: b i Objectives: /i /b This study aimed to investigate the feasibility and effects of intramuscular injections of autologous bone marrow cells (BMC) combined with off-pump coronary artery bypass grafts (OPCAB) on improving cardiac function in chronic myocardial infarction patients. b i Methods: /i /b Ninety patients with chronic myocardial infarction were prospectively enrolled and randomized to an OPCAB with saline or an OPCAB with BMC-treatment group. After finishing CABG, patients received injections of BMC or saline into the marginal area of the infarct. The primary endpoint was incidence of emergent adverse events within 6 months. b i Results: /i /b There were no differences between the control and BMC-treated groups in baseline ejection fractions (EF) or wall motion score indices (WMSI) in the affected segments. At the 6-month follow-up, the ejection fraction was significantly increased in the BMC-treated group compared to controls (47.58 w 6.34 vs. 40.11 w 7.42 p 0.05), whereas the WMSI were significantly decreased (1.25 w 0.32 vs. 1.54 w 0.53 p 0.05), with no occurrences of life-threatening arrhythmias or death. The addition of BMC injections to OPCAB treatment increased regional perfusion to the marginal infarct area. b i Conclusion: /i /b These results demonstrate that BMC transplant is beneficial to the cardiac function with no adverse effects, and therefore a safe and feasible adjunct therapy providing beneficial effects in clinical practice. i 2014 S. Karger AG, Basel
Publisher: Elsevier BV
Date: 10-2011
Publisher: Hindawi Limited
Date: 09-2022
DOI: 10.1155/2022/6248779
Abstract: Background. Inflammation plays important roles during myocardial infarction (MI). Macrophage polarization is a major factor that drives the inflammatory process. Our previous study found that RNA polymerase II subunit 5-mediating protein (RMP) knockout in cardiomyocytes caused heart failure by impairing mitochondrial structure and function. However, whether macrophage RMP plays a role in MI has not been investigated. Methods. Macrophage RMP-knockout in combination with a mouse model of MI was used to study the function of macrophage RMP in MI. Next, we modified bone marrow-derived macrophages (BMDMs) by plasmid transfection, and the BMDMs were administered to LysM-Cre/DTR mice by tail vein injection. Immunoblotting and immunofluorescence were used to detect macrophage polarization, fibrosis, angiogenesis, and the p38 signaling pathway in each group. Results. Macrophage RMP deficiency aggravates cardiac dysfunction, promotes M1 polarization, and inhibits angiogenesis after MI. However, RMP overexpression in macrophages promotes M2 polarization and angiogenesis after MI. Mechanistically, we found that RMP regulates macrophage polarization through the heat shock protein 90– (HSP90–) p38 signaling pathway. Conclusions. Macrophage RMP plays a significant role in MI, likely by regulating macrophage polarization via the HSP90–p38 signaling pathway.
Publisher: Cold Spring Harbor Laboratory
Date: 27-10-2023
Publisher: Elsevier BV
Date: 08-2013
DOI: 10.1016/J.CARDFAIL.2013.06.001
Abstract: A symptomatic reduction in left ventricular ejection fraction (LVEF) is the main reason for postoperative heart failure after valve replacement surgery. However, postoperative heart failure occurs in patients with normal preoperative LVEF. Therefore, we examined clinical and echocardiographic data of patients with rheumatic heart disease to determine additional risk factors for low LVEF in the postoperative period. Ninety-seven patients with rheumatic heart disease (RHD) who underwent mitral valve replacement for severe mitral valve stenosis were included retrospectively in this study. All patients had normal LVEF before surgery. Patients were ided into 2 groups based on postoperative LVEF 6 months after surgery. Groups A had normal postoperative LVEF (82 cases, 84.5%), and group B had low postoperative LVEF (15 cases, 15.5%). Clinical and electrocardiographic data were collected to determine risk factors for deterioration in cardiac function. Multivariate analysis revealed that preoperative low systolic peak velocities at the lateral tricuspid annulus (St) and no or mild aortic stenosis were independent risk factors for cardiac deterioration in patients with normal preoperative LVEF. In iduals with preoperative St ≤ 4.8 cm/s were more likely to develop lower LVEF at follow-up (χ(2) = 7.54 P = .006 odds ratio 5.03, 95% confidence interval 1.31-20.82). All 15 patients who had normal preoperative LVEF but abnormal postoperative LVEF had no or only mild aortic valve stenosis. Decreased right ventricular function and no or mild aortic stenosis were independent risk factors for low LVEF at follow-up in patients with RHD who had normal preoperative LVEF. The velocity of the tricuspid valve ring should be included in preoperative evaluations to improve the accuracy of postsurgical prognosis and clinical decision making.
Publisher: Georg Thieme Verlag KG
Date: 10-04-2015
Abstract: To investigate the perioperative features of aged patients undergoing off-pump coronary artery bypass grafting (OPCABG) surgery, and identify the perioperative effect of advanced age on OPCABG. A total of 61 aged patients and 585 younger patients from August 2013 to June 2014 were enrolled in this study. The perioperative features were summarized, and the effects of advanced age on intraoperative variables, as well as the postoperative complications were identified using logistic regression analysis. The anastomosis time of the target coronary artery and intraoperative dosage of vasoconstrictor drugs was significantly longer or higher in the aged patients. The incidence of the postoperative complications, such as atrial fibrillation, repetitive mechanical ventilation, gastrointestinal dysfunction, and renal insufficiency, were significantly higher in the aged patients. The intubation time and postoperative hospital stay were significantly longer in the aged patients. No significant difference was found between the two groups in cardiocerebrovascular accident and mortality. Multivariate logistic regression analysis revealed advanced age was the independent risk factor for coronary artery anastomosis time, vasoconstrictor dosage, repeated mechanical ventilation, atrial fibrillation, gastrointestinal dysfunction, as well as the intubation time and hospital stay. OPCABG in aged patients was safe and effective for avoiding a significant increase for cardiocerebrovascular accident and mortality. Relatively, the tolerance of aged heart to stimulation was poor. Atrial fibrillation, repetitive mechanical ventilation, and gastrointestinal dysfunction were more likely to occur in aged patients. Advanced age made intubation time and hospital stay prolonged significantly.
Publisher: Elsevier BV
Date: 09-2016
Publisher: Wiley
Date: 15-03-2022
DOI: 10.1002/CLC.23811
Abstract: Atrial fibrillation (AF) is common arrhythmia in valvular heart disease (VHD) and is associated with adverse outcomes. To evaluate the left atrial (LA) function in patients with AF‐VHD by cardiovascular magnetic resonance imaging feature tracking (CMR‐FT) using LA strain ( ε s / ε e / ε a ) and their corresponding strain rate (SRs/SRe/SRa). This was a retrospective cross‐sectional inter‐reader and intra‐reader reproducibility conducted from July 1, 2020, to January 31, 2021. A total of 39 patients with AF‐VHD (rheumatic heart valvular disease [RHVD] [ n = 22], degenerative heart valvular disease [DHVD] [ n = 17]) underwent MRI scans performed with drug‐controlled heart rate before correcting the rhythm and valves through maze procedure. Fifteen participants with normal cardiac MRI were included as healthy control. ε s /SRs, ε e /SRe, and ε a /SRa, corresponding to LA reservoir, conduit, and booster‐pump function, were assessed using Feature Tracking software (CVI42 v5.12.1). Compared with healthy controls, LA global strain parameters ( ε s / ε e / ε a /SRs/SRe/SRa) were significantly decreased (all p 0.001), while LA size and volume were increased in AF‐VHD group (all p 0.001). In the subgroup, RHVD group showed lower LA total ejection fraction (LATEF) and strain data than DHVD group (12.6% ± 3.3% vs. 19.4 ± 8.6, p = 0.001). Decreased LATEF was significantly related to altered LA strain and strain rate, especially in ε s , ε e , and SRs (Pearson/Spearman r/ρ = 0.856/0.837/0.562, respectively all p 0.001). Interstudy and intrastudy reproducibility were consistent for LA volumetry and strain parameters (intraclass correlation coefficient: 0.88–0.99). CMR‐FT can be used to assess the LA strain parameters, and identify LA dysfunction and deformation noninvasively, which could be a helpful functional imaging biomarker in the clinical treatment of AF‐VHD.
Publisher: Springer Science and Business Media LLC
Date: 02-08-2017
DOI: 10.1038/S41598-017-07559-0
Abstract: Endothelial cell injury can promote the development of various cardiovascular diseases, thus, fully understanding the mechanisms underlying the maintenance of vascular endothelial cell homoeostasis may help prevent and treat cardiovascular disease. Kaiso, a zinc finger and BTB domain containing transcription factor, is key to embryonic development and cancer, but how Kaiso interacts with vascular endothelium is not fully understood. We report that Kaiso has an anti-apoptotic function in human umbilical vein endothelial cells (HUVECs) and human microvascular endothelial cells (HMEC-1s). Overexpression of Kaiso significantly increased cell viability and inhibited hydrogen peroxide-induced apoptosis. Furthermore, Kaiso increased expression of B-cell CLL/lymphoma 2 (BCL2) and reduced expression of BCL2-associated X protein (BAX) and BCL2-interacting killer (BIK) by differentially regulating gene promoter activity. Methylated DNA and specific Kaiso binding site (KBS) contributed to gene regulatory activity of Kaiso. In addition, p120ctn functioned cooperatively in Kaiso-mediated transcriptional regulation.
Publisher: Elsevier BV
Date: 06-2016
DOI: 10.1016/J.CRYOBIOL.2016.03.011
Abstract: Hypothermia has positive and negative consequences on the body. Hypothermia depresses myocardial contraction, conduction, and metabolic rate in the heart. However, little is known about the underlying molecular mechanisms. Herein, we compared the gene expression of human adult ventricular cardiomyocytes (AC16) under hypothermia to find differences between different temperatures, and elucidate the candidate genes that may play important roles in the response to hypothermia. A total of 2413 differentially expressed genes (DEGs) were identified by microarray hybridization, which provided abundant data for further analysis. Gene Ontology (GO) enrichment analysis revealed that genes related to transcription, and protein and lipid metabolism were significantly enriched. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that DEGs were significantly enriched in TGF-β pathway and cytokine-cytokine receptor interaction, which may play important roles in changes affected by hypothermia. A set of transcription factors (TFs) (CPBP, Churchill, NF-AT1, GKLF, SRY, ZNF333, ING4, myogenin, DRI1 and CRX) was recognized to be the functional layer of key nodes, which mapped the signal of hypothermia to transcriptome. The identified DEGs, pathways and predicted TFs could facilitate further investigations of the detailed molecular mechanisms.
Publisher: Impact Journals, LLC
Date: 17-03-2017
Publisher: Hindawi Limited
Date: 09-2013
DOI: 10.1111/JOCS.12202
Abstract: Common atrium (CA) is a rare congenital heart defect. We reviewed our experience of surgical treatment of CA and summarize the clinical features of CA and the key techniques for surgical correction. Between August 1984 and August 2010, 37 consecutive cases of CA underwent corrective surgery. There were no clinical findings of Down, asplenia-polysplenia or Ellis-van Creveld syndromes in all cases. Mitral valvuloplasty was performed in 34 cases, and tricuspid valvuloplasty in 20 cases. Complete closure of a mitral cleft was required in 32 cases. All new atrial septa were reconstructed using patches. Follow-up period ranged from 1 to 20 years. There were no hospital deaths or conduction system block. After surgery, mild mitral insufficiency was observed in only one case. Two cases had moderate-severe mitral insufficiency at postoperative years 1 and 3, respectively, that required mitral valve replacements. One patient died of low cardiac output syndrome after reoperation. Long-term survival after surgical correction of CA is good. Routine closure of a cleft in the mitral valve is very important for successful surgery.
Publisher: Genetics and Molecular Research
Date: 2014
Publisher: No publisher found
Date: 23-02-2011
Abstract: Aim: Reducing lung injury during cardiopulmonary bypass (CPB) is important for patients' recovery. The present study was designed to research convenient and effective pulmonary artery perfusion mode during CPB in an animal model.Methods: Twelve healthy mongrel dogs were randomly ided into 2 groups: a control group and a perfusion group designed to simulate clinical CPB-induced lung injury. During CPB, pulmonary artery perfusion with modified lowpotassium dextran (LPD) solution was performed immediately after the initiation of ischemia and before reperfusion for 3 to 4 minutes each time, with pressure maintained at 15 to 20 mmHg animals in the control group were not perfused. After pulmonary reperfusion, the changes in pulmonary function and tissue biochemical data were determined.Results: Compared with the control group, lung compliance, oxygenation, and vascular resistance after reperfusion were significantly improved in the perfusion group. The malonaldehyde concentration, neutrophil sequestration ratio, and tissue water content also decreased significantly in the perfusion group.Conclusion: The pulmonary artery perfusion mode used in this experiment could relieve CPB-induced lung injury effectively. Improving cellular tolerance to hypoxia and decreasing inflammatory reaction may be the important mechanisms. Moreover, this mode is convenient and does not interfere with the intended operations, which is promising for clinical use.
Publisher: Wiley
Date: 28-06-2014
DOI: 10.1111/ECHO.12652
Abstract: Early death following coronary artery bypass graft (CABG) surgery tends to occur in coronary heart disease (CHD) patients with significantly decreased left ventricular function. The clinical data of 231 patients with preoperative left ventricular ejection fraction (LVEF) ≤ 35% who underwent CABG were retrospectively analyzed from June 2007 to October 2012. The patients were ided into 2 groups: group A contained 39 patients who suffered early postoperative death and group B contained 192 patients who had a successful CABG outcome. Multivariate analysis demonstrated that only significantly decreased preoperative right ventricular (RV) diastolic function (increase in Et/Et') and lack of suitable target bypass vessels were independent risk factors for early death after CABG surgery in patients with severely impaired left ventricular function (P = 0.003 and 0.002, respectively). Other factors, including age, intra-aortic balloon pump (IABP) implantation, ischemic mitral regurgitation (IMR) treatment, left atrial internal diameter, and end-diastolic left ventricular internal diameter, were not associated with early death following CABG. Preoperative Et/Et' ≥ 10 was significantly associated with early death after CABG in patients with severely impaired left ventricular function (χ(2) = 11.55, P < 0.001, odds ratio [OR] = 17.54, 95% confidence interval [CI]: 2.12-383.16). Decreased preoperative RV diastolic function and lack of suitable target bypass vessels are independent risk factors for early death following CABG in patients with severely impaired left ventricular function. Therefore, assessment of preoperative RV diastolic function will be helpful in predicting early death after CABG in these patients. Additionally, Et/Et' ≥ 10 is significantly associated with early death after CABG.
Publisher: Elsevier BV
Date: 02-2018
DOI: 10.1016/J.JTCVS.2017.07.084
Abstract: To evaluate the safety and efficacy of the addition of the cut-and-sew Maze III procedure (CSM) for mitral valve replacement (MVR) in patients with atrial fibrillation (AF) associated with rheumatic mitral valve disease (RMVD). A total of 130 patients with persistent or long-standing persistent AF associated with RMVD were assigned at random to either the CSM plus MVR (Maze III) group or MVR alone (non-Maze) group. The primary endpoint was a composite of freedom from stroke and death at 1 year. There were no significant differences between the Maze III and non-Maze groups in terms of major complications and in-hospital mortality. One-year freedom from stroke or death was better in the Maze III group compared with the non-Maze group (P = .0028 hazard ratio, 0.2653 95% confidence interval, 0.1122 to 0.6270). The risk of AF recurrence in the Maze III group was 0.002-fold that in non-Maze group (P = .000). Addition of the CSM to an MVR procedure can decrease the risk of stroke or death and high sinus rhythm at 1 year without increasing the operative risk. CSM is a safe and effective approach to treating AF associated with RMVD.
Publisher: Royal Society of Chemistry (RSC)
Date: 2022
DOI: 10.1039/D2FO00966H
Abstract: Polydatin attenuates cardiac remodeling and mitochondrial dysfunction in an alcoholic cardiomyopathy model via SIRT6 signaling.
Publisher: Wiley
Date: 04-08-2023
DOI: 10.1002/CLC.24110
Abstract: Mitral annular calcification (MAC) by computed tomography (CT) is reported as an independent predictor of poor outcomes. However, it currently remains unclear if quantitative MAC parameters provide more value for mitral valve disease (MVD) management, therefore, we examined the prognostic value of MAC scores using noncontrast cardiac‐CT in MVD patients. Between January 2020 and December 2021, we prospectively enrolled 300 consecutive patients with MVD (MAC‐present = 80 and MAC‐absent = 220) undergoing preoperative cardiac‐CT and mitral valve (MV) surgery. Noncontrast cardiac‐CT images were used to qualitatively detect MAC (present or absent) and evaluate MAC scores. For analyses, we also collected baseline clinical data, intraoperative conversion (from MV repair to MV replacement), and follow‐up arrhythmia data. Compared with the MAC‐absent group, MAC‐present patients were older (62 ± 7 vs. 58 ± 9 years, p .001), mostly women (55% vs. 39.5%, p = .017), and also had aortic valve calcification (57.5% vs. 23.2%, p .001), mitral stenosis (82.5% vs. 61.8%, p .001), atrial fibrillation (30% vs. 11.8%, p .001), and larger left atrial end‐diastolic dimension (LADD, 49 [44–56] versus 46 [41–50], p = .001]. Furthermore, MAC‐present patients underwent more MV replacements (61.8% vs. 82.5%, p = .001) and experienced a higher intraoperative conversion prevalence (11.8% vs. 61.3%, p .001). Multiple logistic regression analyses showed that the female gender (odds ratio [OR]/95% confidence interval [CI]/ p = 2.001/1.042–3.841/0.037) and MAC scores (OR/95% CI/ p = 10.153/4.434–23.253/ p .001) were independent predictors of intraoperative conversion. During a follow‐up of 263 ± 134 days, MAC‐present patients had more arrhythmias (42.5% vs. 9.5%, p .001). Also, MAC‐scores (hazard ratio [HR]/95% CI/ p = 6.841/3.322–14.089/ p .001) and LADD (HR/95% CI/ p = 1.039/1.018–1.060/ p .001) were independently associated with arrhythmias by Cox regression analyses. Noncontrast cardiac CT‐derived MAC‐scores showed a high risk for intraoperative conversion and follow‐up arrhythmias in MVD‐patients.
Publisher: Elsevier BV
Date: 02-2012
DOI: 10.1016/J.ATHORACSUR.2011.10.001
Abstract: Right-side heart function is essentially externalized during extracardiac total cavopulmonary connection. The Fontan procedure has a certain impact on pulmonary hemoperfusion and may explain various postsurgical complications. In this study, alterations of pulmonary perfusion in patients undergoing the Fontan procedure were analyzed at the 5-year postoperative mark by radionuclide imaging and angiocardiography, and results of both methods were compared. For 43 post-Fontan patients, perfusion ratios of each lung segment were calculated based on radionuclide imaging data. The pulmonary vascular resistance and pulmonary artery index of each patient were also calculated from right angiocardiographic measurements. The radionuclide count and advantage perfusion ratio of right lung at follow-up did not differ significantly from early postoperative values (t=0.38, p>0.05 t=1.12, p>0.05), and superior/inferior vena cava perfusion ratios were stable (t=0.88, p>0.05 t=0.74, p>0.05). The superior/inferior segment perfusion ratio of the whole lung declined significantly (t=2.54, p<0.05), while that of the dorsal lung segment rose significantly (t=2.16, p<0.05). Compared with early postoperative status, the pulmonary arterial index of patients at follow-up were significantly increased (t=2.41, p<0.05), while small pulmonary vascular resistances declined significantly (t=2.08, p<0.05 t=2.69, p 0.05). The early angiographic and radionuclide perfusion studies of 5 patients did not match. After the Fontan procedure, hypostatic redistribution of pulmonary blood flow is characteristic. The weak pulse of blood, in the absence of ventricular ejection, can promote pulmonary vascular changes, but at later (intermediate) follow-up, the decline in vascular resistance that results carries no benefit in terms of blood perfusion or oxygenation. Microcirculatory arteriovenous shunting is the likely cause. In this study of functional pulmonary hemoperfusion, radionuclide imaging was deemed superior to angiocardiography.
Publisher: SAGE Publications
Date: 02-2009
Abstract: Cardiopulmonary adaptation during exercise was compared in patients with an extracardiac total cavopulmonary connection and controls with biventricular repair of Fallot's tetralogy. Heart rate, blood pressure, respiratory frequency, and transcutaneous oxygen saturation increased with treadmill exercise intensity below grade 3 in patients who had undergone extracardiac total cavopulmonary connection. When exercise intensity exceeded grade 4, blood pressure and oxygen saturation decreased continuously, respiratory rate kept increasing, and heart rate showed no significant change. In cases of fenestrated cavopulmonary connection, heart rate peaked at grade 5 exercise intensity, and blood pressure at grade 4 but both peaked at grade 3 in nonfenestrated patients. During all exercise testing, fenestrated patients had a higher respiratory rate but lower oxygen saturation than those without fenestration. Exercise tolerance was below normal after a cavopulmonary connection, but patients still adapted to exercise below grade 3 with appropriate increases in heart rate and respiratory rate. Due to insufficient right heart systems, patients with a cavopulmonary connection showed obvious exercise limitation at exercise intensity grade 3 or more. Total exclusion of the right heart system may also have adverse effects on the sinoatrial node, leading to impaired heart rate regulation.
Publisher: Wiley
Date: 14-06-2021
DOI: 10.1111/JCMM.16691
Abstract: Although reperfusion is the most effective therapy for patients with acute myocardial infarction, reperfusion injury limits the therapeutic effects of early reperfusion. Oxidative stress plays a crucial role in myocardial ischaemia/reperfusion (I/R) injury. Melatonin, a circulating hormone, is well‐known as an antioxidant in cardiovascular diseases. In this short communication, we show that melatonin significantly improves post‐ischaemic cardiac function, reduces infarct size and decreases oxidative stress. Furthermore, melatonin markedly increases AMPK activation and Nrf2 nuclear translocation. Nevertheless, these melatonin‐induced changes are abrogated by compound C. In addition, ML‐385, an Nrf2 inhibitor, also withdraws the antioxidative effects of melatonin but has little effect on AMPK activation. In conclusion, our results demonstrate that melatonin alleviates myocardial I/R injury by inhibiting oxidative stress via the AMPK/Nrf2 signalling pathway.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 10-2022
DOI: 10.1161/CIRCEP.122.011160
Abstract: Postoperative atrial fibrillation (POAF) is one of the most common complications of cardiac surgery, but the underlying factors governing POAF are not well understood. The aim of this study was to investigate the efficacy of berberine administration on POAF. We conducted a randomized, double-blind, placebo-controlled trial with patients who underwent isolated coronary artery bypass grafting in China to study the impact of oral berberine on the incidence of POAF. A total of 200 patients who underwent coronary artery bypass grafting were randomized into the berberine group (n=100) and the placebo group (n=100). All patients underwent 7-day continuous telemetry and Holter monitoring. The primary outcome was the incidence of POAF at 7 days. Secondary outcomes included clinical outcomes, POAF burden, intestinal endotoxin, and serum inflammatory biomarker levels. The POAF incidence was reduced from 35% to 20% under berberine treatment (hazard ratio, 0.5 [95% CI, 0.29–0.78] P =0.0143). Perioperative mortality and morbidity did not differ between the 2 groups. POAF burden and the dose of amiodarone were significantly reduced in the berberine group. Oral berberine significantly decreased lipopolysaccharide, CRP (C-reactive protein), and IL (interleukin)-6 levels. Elevated lipopolysaccharide after surgery has been associated with POAF. Our results showed that administration of berberine may be effective for reducing the occurrence of POAF after coronary artery bypass grafting. URL: www.chictr.org.cn Unique identifier: ChiCTR2000028839.
Publisher: No publisher found
Date: 23-02-2012
Abstract: b Introduction: /b This study was conducted to address whether staged surgical intervention or primary repair would be preferred for treating patients with tetralogy of Fallot and small left ventricle. b Methods: /b We retrospectively assessed 28 patients with tetralogy of Fallot and small left ventricle at the Chinese PLA 208th Hospital, Changchun, between January 2005 and December 2008. Of this cohort, 11 patients had undergone a systemic-to-pulmonary arterial shunt with a polytetrafluoroethylene interposition graft (off pump), followed by ancillary repair procedures as a surgically staged group the remaining 17 patients underwent primary intracardiac repair via cardiopulmonary bypass. The oxygen level as measured by pulse oximetry (SpO2), the McGoon ratio, and the left ventricular end-diastolic volume index (LVEDVI) were measured before shunt procedures and at 6 to 18 months afterwards. All data were analyzed statistically with the paired Student t test. The 2 groups were compared with respect to LVEDVI values and McGoon indices at baseline by the independent t test. b Results: /b None of the patients died as a direct result of the surgery, but 1 fatality due to pneumonia occurred 4 months after shunting. Mean postshunt values for SpO2, the McGoon ratio, and the LVEDVI increased significantly from 76.8% � 9.0% to 87.5% � 2.4% (P .01), from 1.42 � 0.27 to 1.62 � 0.32 (P .05), and from 20.1 � 7.0 mL/m2 to 34.3 � 7.4 mL/m2 (P .01), respectively. Nine patients were fully repaired within the 6- to 18-month time frame after shunting, while 1 patient awaited definitive surgery for pulmonary hypoplasia. In the primary-repair group, in which the increases the LVEDVI and McGoon ratio were comparatively higher, 1 patient died of hypoxemia. b Conclusion: /b A LVEDVI 20 mL/m2 may be an indication for primary repair in patients with tetralogy of Fallot. With values mL/m2, staged procedures (ie, shunt with a polytetrafluoroethylene interposition graft) can promote left ventricle development and allow safe transition to the final repair.
Publisher: Public Library of Science (PLoS)
Date: 23-06-2014
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 02-2012
Publisher: Saudi Medical Journal
Date: 03-2017
Publisher: Springer Science and Business Media LLC
Date: 03-03-2013
Abstract: Diabetes mellitus (DM) exacerbates coronary artery disease (CAD) morbidity and mortality. Mesenchymal stem cells (MSCs) play an important therapeutic role in myocardial ischemic injury. However, little is known about changes in the cardioprotective characteristics of MSCs from patients with DM. Sternal bone marrow aspirates were taken at the time of coronary artery bypass graft surgery. The morphology and growth characteristics of hMSCs were observed in passage 3. Differences in gene expression profiling were measured by Affymetrix GeneChipHuman Genome U133 Plus 2.0 Arrays. Forty two adult male rats with experimentally CAD were randomized into three groups. MSCs from patients with CAD+DM or CAD were injected into the infarcted myocardium. Control animals received culture medium. Echocardiography, TUNEL, immunohistochemistry and Western-blot analysis were performed 4 weeks after transplantation. Growth curves showed that proliferation of hMSCs in the CAD+DM group was significantly lower than in the CAD group. Nine transcripts of genes related to apoptosis containing Bcl-2 were found to differentiate the two groups. Transplantation of hMSCs in the infarcted border zone improved cardiac function, but DM partly impaired this effect. Similar results were observed from TUNEL, immunohistochemistry and Western-blot analysis. hMSCs from patients with CAD+DM and CAD alone both have proliferative properties. Transplantation of hMSCs ameliorate heart function, but proliferative ability and myocardial protection decrease significantly in MSCs obtained from patients with CAD+DM compared with cultures from patients with CAD alone, possibly as a result of differences in Bcl-2 protein expression and reduced anti-apoptosis.
Publisher: Genetics and Molecular Research
Date: 2014
Publisher: Georg Thieme Verlag KG
Date: 05-03-2015
Abstract: Though maze III procedure is an effective surgical treatment for atrial fibrillation (AF), the complexity and complications prevent its widespread application. Radiofrequency ablation (RA) has become an accepted therapy, but its chronic effects are still unclear. This retrospective clinical study describes our experience of RA and vagal denervation (VD) in surgical treatment of long-standing AF associated with rheumatic heart disease (RHD) during a 5-year follow-up. Between June 2006 and December 2007, a total of 173 consecutive patients with long-standing AF-associated RHD underwent mitral valve replacement and ablation maze procedure. In total, 92 cases had RA alone and 81 had RA + VD. Patients were followed up with clinical examination and electrocardiography, and the data were analyzed by multivariable analysis with Cox hazard model. The average follow-up time was 5.0 ± 0.6 years. Multivariable analysis with Cox hazard model revealed that the duration of AF, the size of the left atrium, and tricuspid regurgitation are risk factors for AF recurrence. In addition, long-standing AF ≥ 7 years, left atrium diameter ≥ 58 mm, and severe tricuspid regurgitation may increase the risk of AF recurrence by 2.16-, 2.37-, and 2.67-fold, respectively. Although the freedom from AF during 2 to 5 postoperative years in the RA and RA + VD groups were similar, the percentage of antiarrhythmic drug therapy was higher in the RA group during the early postoperative period (4th month, 54.1 vs. 34.7%, p = 0.017 5th month, 39.2 vs. 21.3%, p = 0.018 6th month, 23.0 vs. 10.7%, p = 0.044). Furthermore, the percentage of those free from AF was lower during the 1st year (6th month, 82.2 vs 93.8%, p = 0.023 1st year, 76.1 vs. 89.9%, p = 0.019). RA is effective for the surgical treatment of long-standing AF associated with rheumatic valve disease. Though vagal denervation helped to maintain a stable sinus rhythm at an early stage, there was no additional benefit after the 1st year of follow-up.
Publisher: MDPI AG
Date: 13-02-2023
DOI: 10.3390/JCM12041493
Abstract: Background: Post-operative atrial fibrillation (POAF) is one of the most common complications of cardiac surgery. However, the underlying mechanism is not well understood. Alterations in the gut microbiota are associated with the development of atrial fibrillation (AF). The aim of this study was to explore the relationship between gut microbiota and POAF. Methods: Fecal s les were collected before surgery from 45 patients who underwent coronary artery bypass grafting with POAF and 90 matched patients without POAF (1:2). 16S rRNA sequencing was used to detect the microbiome profiles of 45 POAF patients and 89 matched patients (one s le in the no-POAF group was deleted owing to low quality after sequencing). Plasma 25-hydroxy vitamin D level was measured by ELISA. Results: Compared to the patients without POAF, gut microbiota composition was remarkably changed in the patients with POAF, with an increase in Lachnospira, Acinetobacter, Veillonella and Aeromonas, and a decrease in Escherichia–Shigella, Klebsiella, Streptococcus, Brevundimonas and Citrobacter. Furthermore, plasma 25-hydroxy vitamin D levels were decreased in POAF patients and negatively correlated with an abundance of Lachnospira. Conclusions: The gut microbiota composition between patients with and without POAF is significantly different, implying that gut microbiota may play a role in the pathogenesis of POAF. Further studies are needed to fully clarify the role of gut microbiota in the initiation of AF.
Publisher: Georg Thieme Verlag KG
Date: 25-11-2010
Abstract: The aim of the study was to investigate whether functional changes and structural remodeling occurs in the microvascular bed of the pulmonary circulation under nonpulsatile flow perfusion. An animal model of unilateral nonpulsatile flow in the right lung was established in dogs. Streptavidin-biotin enzyme complex (SP method) was used to detect the expression of endothelial nitric oxide synthase (eNOS) in vascular endothelial cells and the apoptosis-related protein Fas in smooth muscle cells of the pulmonary artery of both lungs, and structural changes of the arterioles in the capillary bed of both lungs were observed under light microscope. eNOS expression in right lung arterioles with nonpulsatile flow perfusion was significantly lower than in the left lung (10,846.7 ± 177.8 vs. 13,136.1 ± 189.6 T = 2.24, P < 0.05). Expression of the apoptosis-related protein Fas in smooth muscle cells of the arteriole of the right lung was significantly higher than in the left lung (14,254.1 ± 217.1 vs. 11,976.7 ± 195.7 T = 2.16, P < 0.05). Image analysis of pulmonary arterioles showed that the ratio of vascular wall thickness and the external vessel diameter (13.64% ± 12.8% vs. 14.96% ± 13.1%) and the ratio of vascular wall area and the total vessel area (46.4% ± 11.7% vs. 47.8% ± 12.2%) of the right lung were significantly lower than in the left lung. Long-term nonpulsatile flow perfusion of the Fontan circulation can decrease the synthesis of eNOS in endothelial cells of the pulmonary vessels, increase the apoptosis of smooth muscle cells of the arteriole wall, and lead to arterial venous conversion and pulmonary vessel remodeling.
Publisher: Public Library of Science (PLoS)
Date: 04-04-2014
Publisher: Wiley
Date: 05-01-2015
DOI: 10.1002/JCPH.411
Abstract: This study aimed to investigate the impact of different doses of atorvastatin on contrast-induced acute kidney injury (CI-AKI) in patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI) requiring contrast media by performing a meta-analysis. We searched the PubMed, EMBASE, Cochrane Library, Wanfang database, China National Knowledge Infrastructure, and VIP database through April 2014. Only randomized controlled trials (RCTs) comparing short-term high-dose atorvastatin with low-dose atorvastatin on CI-AKI were selected. The main outcomes were the change of acute kidney injury markers and the incidence of contrast-induced nephropathy (CIN). We combined 14 RCTs consisting of 1,689 patients. Compared with the low-dose atorvastatin, high-dose atorvastatin treatment was associated with a reduction in serum creatinine levels (weighted mean differences [WMD]-0.1 mg/dL 95%CI -0.14 to -0.05). In addition, high-dose atorvastatin treatment was also associated with a lower incidence of CIN (risk ratios 0.41 95%CI 0.29-0.56). This meta-analysis suggests that short-term high-dose atorvastatin therapy appears to be superior to the low-dose atorvastatin in preventing CI-AKI among patients undergoing CAG/PCI requiring contrast media.
Publisher: Spandidos Publications
Date: 15-02-2017
Publisher: Georg Thieme Verlag KG
Date: 09-02-2016
Publisher: Springer Science and Business Media LLC
Date: 24-11-2015
Publisher: Hindawi Limited
Date: 2018
DOI: 10.1155/2018/2750695
Abstract: Diabetes exacerbates oxidative/nitrative stress during myocardial ischemia-reperfusion (MI/R) injury. Recent studies highlighted the cardioprotective actions of polydatin. However, its effect on diabetic MI/R injury and the underlying mechanisms remain unknown. This work was undertaken to evaluate the effect of polydatin on diabetic MI/R injury with a focus on Notch1/Hes1 signaling and myocardial oxidative/nitrative stress. Streptozotocin- (STZ-) induced diabetic rats were administered with polydatin (20 mg/kg/d) in the absence or presence of DAPT (a γ -secretase inhibitor) or LY294002 (a PI3K/Akt inhibitor) and then subjected to MI/R injury. Polydatin administration preserved cardiac function and reduced myocardial infarct size. Moreover, polydatin ameliorated myocardial oxidative/nitrative stress damage as evidenced by decreased myocardial superoxide generation, malondialdehyde, gp91 phox expression, iNOS expression, NO metabolite level, and nitrotyrosine content and increased eNOS phosphorylation. However, these effects were blocked by DAPT administration. DAPT also inhibited the stimulatory effect of polydatin on the Notch1/Hes1-Pten/Akt signaling pathway in a diabetic myocardium. Additionally, LY294002 not only abolished polydatin’s antiapoptotic effect but also reversed its inhibitory effect on myocardial oxidative/nitrative stress. Polydatin effectively reduced MI/R injury and improved left ventricular functional recovery under diabetic condition by ameliorating oxidative/nitrative stress damage. Importantly, Notch1/Hes1-mediated activation of Pten/Akt signaling played a crucial role in this process.
Publisher: S. Karger AG
Date: 2014
DOI: 10.1159/000360393
Abstract: b i Objectives: /i /b Mesenchymal stem cells (MSCs) have limited clinical therapeutic effects in older myocardial infarction (MI) patients. Thus, whether younger MSCs might confer greater protection is worth investigating. b i Methods: /i /b Human MSCs (hMSCs) were isolated before coronary artery bypass graft surgery and growth characteristics of hMSCs at passage 3 were observed. Vascular endothelial growth factor (VEGF) and Bcl-2 mRNA and protein expression from hMSCs were measured. In vivo, 45 adult male rats with MI were randomized to receive one of three treatments: old hMSCs, young hMSCs or culture medium (control) transplanted into infarcted myocardium. Echocardiography, TUNEL, immunohistochemistry and Western blot were used to assess results. b i Results: /i /b hMSC proliferation in the old group was significantly lower than the young group. VEGF decreased 35% and Bcl-2 decreased more than 60% at the mRNA level VEGF and Bcl-2 protein were decreased in the old versus the young group. hMSC transplantation may improve cardiac function, but MSC source may affect therapeutic efficacy. Similar data were obtained from TUNEL, immunohistochemistry and Western blot. b i Conclusion: /i /b Transplantation of hMSCs improves heart function, but proliferative ability and myocardial protection decrease with older MSCs, likely due to differences between VEGF and Bcl-2 expression and reduced anti-apoptosis.
Publisher: No publisher found
Date: 13-10-2011
Abstract: b Objective: /b We aimed to investigate the initial experience of endoscopic vein harvesting (EVH) for coronary artery bypass grafting (CABG) in Chinese patients. b Methods: /b Forty patients scheduled for isolated CABG were prospectively randomized into an EVH group (n = 20) and an open vein harvesting (OVH) group (n = 20). Clinical data were collected, and all of the vein grafts were assessed by macroscopic appearance, histologic quality (endothelial integrity), and functional characteristics of endothelial nitric oxide synthase. b Results: /b The 2 groups were similar with respect to hospital mortality (EVH group, 0 OVH group, 1 i P /i = 1). There were no postoperative myocardial infarctions in either group and no deaths or reinterventions in either group during the follow-up period. Harvesting times in the 2 groups were similar (EVH, 12.15 � 2.32 min OVH, 12.55 � 2.11 min i P /i = .571). Three patients in the EVH group were converted to a partly open or skin-bridge technique. Electrocautery at least 2 mm distal to the origin of the side branch was the safety margin. b Conclusions: /b The use of EVH in Chinese patients was not related to adverse events and may be safely used for CABG procedures. Preoperative duplex mapping, systemic heparinization before harvesting, minimal surgical manipulation, and sectioning of side branches at least 2 mm distal to the origin may help improve the quality of vein grafts harvested with EVH and maximize the benefit of this less-invasive technique.
Publisher: Elsevier BV
Date: 2022
DOI: 10.1016/J.FREERADBIOMED.2021.11.043
Abstract: Mitochondrial reactive oxygen species (ROS) damage and atrial remodeling serve as the crucial substrates for the genesis of atrial fibrillation (AF). Branched-chain amino acids (BCAAs) catabolic defect plays critical roles in multiple cardiovascular diseases. However, the alteration of atrial BCAA catabolism and its role in AF remain largely unknown. This study aimed to explore the role of BCAA catabolism in the pathogenesis of AF and to further evaluate the therapeutic effect of melatonin with a focus on protein kinase G (PKG)-cAMP response element binding protein (CREB)-Krüppel-like factor 15 (KLF15) signaling. We found that angiotensin II-treated atria exhibited significantly elevated BCAA level, reduced BCAA catabolic enzyme activity, increased AF vulnerability, aggravated atrial electrical and structural remodeling, and enhanced mitochondrial ROS damage. These deleterious effects were attenuated by melatonin co-administration while exacerbated by BCAA oral supplementation. Melatonin treatment ameliorated BCAA-induced atrial damage and reversed BCAA-induced down-regulation of atrial PKGIα expression, CREB phosphorylation as well as KLF15 expression. However, inhibition of PKG partly abolished melatonin-induced beneficial actions. In summary, these data demonstrated that atrial BCAA catabolic defect contributed to the pathogenesis of AF by aggravating tissue fibrosis and mitochondrial ROS damage. Melatonin treatment ameliorated Ang II-induced atrial structural as well as electrical remodeling by activating PKG-CREB-KLF15. The present study reveals additional mechanisms contributing to AF genesis and highlights the opportunity of a novel therapy for AF by targeting BCAA catabolism. Melatonin may serve as a potential therapeutic agent for AF intervention.
Publisher: Elsevier BV
Date: 09-2018
DOI: 10.1016/J.IJCARD.2017.12.097
Abstract: Myocardial infarction (MI) is one of the most common causes of cardiac morbidity and mortality. Many evidences suggest that hypothermia have a more pronounced impact as an adjunctive therapy for MI to reduce infarct size. However, the function of long non-coding RNAs (lncRNA) in therapeutic hypothermia for MI remains poorly understood. In this study, we investigated the expression of lncRNA-UIHTC (upregulated in hypothermia treated cardiomyocytes, NONHSAT094064) in ischemic heart tissues. To investigate its function, overexpression of UIHTC was performed by adeno-associated virus vectors after MI model in rat. lncRNA-UIHTC was upregulated in ischemic or injury cardiomyocytes. Overexpression of lncRNA-UIHTC in peri-infarction attenuated cardiac dysfunction in vivo. Mechanistically, lncRNA-UIHTC enhanced the mitochondrial function via upregulation of PGC1α. Moreover, when we knocked down PGC1α, the mitochondrial maximal oxygen consumption and ATP levels enhanced by overexpression of UIHTC were nearly completely restored. Altogether we have provided a new mechanism whereby hypothermia protected heart against ischemic via lncRNA-UIHTC. The UIHTC provided a new potential therapeutic target for MI but prevented the complications of hypothermia.
Publisher: Hindawi Limited
Date: 2015
DOI: 10.1155/2015/176409
Abstract: Objectives. Low survival rate of mesenchymal stem cells (MSCs) severely limited the therapeutic efficacy of cell therapy in the treatment of myocardial infarction (MI). Bcl-xL genetic modification might enhance MSC survival after transplantation. Methods. Adult rat bone marrow MSCs were modified with human Bcl-xL gene (hBcl-xL-MSCs) or empty vector (vector-MSCs). MSC apoptosis and paracrine secretions were characterized using flow cytometry, TUNEL, and ELISA in vitro . In vivo , randomized adult rats with MI received myocardial injections of one of the three reagents: hBcl-xL-MSCs, vector-MSCs, or culture medium. Histochemistry, TUNEL, and echocardiography were carried out to evaluate cell engraftment, apoptosis, angiogenesis, scar formation, and cardiac functional recovery. Results . In vitro , cell apoptosis decreased 43%, and vascular endothelial growth factor (VEGF), insulin-like growth factor-1 (IGF-1), and plate-derived growth factor (PDGF) increased 1.5-, 0.7-, and 1.2-fold, respectively, in hBcl-xL-MSCs versus wild type and vector-MSCs. In vivo , cell apoptosis decreased 40% and 26% in hBcl-xL-MSC group versus medium and vector-MSC group, respectively. Similar results were observed in cell engraftment, angiogenesis, scar formation, and cardiac functional recovery. Conclusions. Genetic modification of MSCs with hBcl-xL gene could be an intriguing strategy to improve the therapeutic efficacy of cell therapy in the treatment of heart infarction.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 23-01-2018
Abstract: Circular RNAs (circRNAs) are pervasively expressed in highly ergent eukaryotes and are stable in body fluids. However, the link between circRNAs and onset of atrial fibrillation (AF) has not previously been investigated. We aimed to identify plasma circRNAs that are able predict AF after cardiac surgery. Plasma circRNA expression profiles were investigated in a total of 769 patients with or without AF after isolated off‐pump coronary artery bypass grafting. First, a circRNA microarray was used to screen 13 617 human circRNAs in plasma s les from patients in the discovery cohort (n=30). A quantitative polymerase chain reaction assay was then applied to evaluate the expression of 9 selected circRNAs in the training cohort (n=365). This approach revealed that hsa_circRNA_025016 was upregulated in patients with new‐onset AF with a high diagnostic accuracy as assessed by the area under the receiver operating characteristic curve (=0.802). Additionally, a satisfactory diagnostic performance of hsa_circRNA_025016 was found in the validation cohort (n=284). Furthermore, Kyoto Encyclopedia of Genes and Genomes biological pathway analysis indicated that hsa_circ_025016 participated in melanogenesis, insulin secretion, and the thyroid hormone signaling pathway. A positive correlation between hsa_circ_025016 and fasting blood glucose was also identified in both cohorts. Hsa_circ_025016 is a potential biomarker for predicting new‐onset AF after isolated off‐pump coronary artery bypass grafting.
Publisher: Wiley
Date: 24-10-2020
DOI: 10.1111/JPI.12698
Publisher: Springer Science and Business Media LLC
Date: 25-01-2018
Publisher: Springer Science and Business Media LLC
Date: 15-12-2016
DOI: 10.1007/S00059-016-4517-2
Abstract: Myocardial infarction is one of the most common causes of death, and the number of in iduals at risk is increasing. A rapid and accurate differential diagnosis of myocardial infarction is crucial for timely interventions and for improvement of the prognosis. However, it is difficult to achieve using current methods. To better manage this condition, improved tools for risk prediction, including more accurate biomarkers, are needed. We studied the expression of microRNA-539 (miR-539) and of MEK protein using a rat model of myocardial infarction. The results of our experiments demonstrated an increase in the expression of miR-539 and a decrease in the expression of MEK. Furthermore, we observed that miR-539 inhibited the expression of MEK through targeting of the 3'UTR of MEK this led not only to suppressed proliferation but also to apoptosis and autophagy of H9C2 cells. Overexpression of miR-539 plays a role in the degree of myocardial infarction. On the basis of our results, we conclude that miR-539 may be a potential therapeutic target for myocardial infarction.
Publisher: Elsevier BV
Date: 02-2023
Publisher: Elsevier BV
Date: 2021
Publisher: Hindawi Limited
Date: 2017
DOI: 10.1155/2017/7951793
Abstract: It has been shown that inflammation and oxidative stress are important factors in postoperative atrial fibrillation (POAF). Angiotensin converting enzyme (ACE) and apelin have a close relationship with inflammation and oxidative stress. The effect of ACE and apelin on POAF after off-pump coronary artery bypass grafting (OPCABG) remains a question. The concentrations of serum ACE, angiotensin II (Ang II), apelin, bradykinin (BK), malondialdehyde (MDA), and C reactive protein (CRP) were measured in the perioperative period of OPCABG. The levels of serum ACE in the POAF group were higher than in the no POAF group both preoperatively and postoperatively. Apelin in the POAF group was lower than in the no POAF group. There was a correlation between serum ACE and apelin. Postoperatively, CRP and MDA in the POAF group were higher than in the no POAF group however, there was no difference before the operation. Preoperative ACE and apelin were both significant and independent risk factors for POAF. In conclusion, the high ACE and low apelin preoperatively led to CRP and MDA being increased postoperatively, which was probably associated with POAF after OPCABG. Apelin may be a new predictor for POAF.
Publisher: Georg Thieme Verlag KG
Date: 24-09-2013
Abstract: To evaluate the development of pulmonary arteries (PAs) in patients with pulmonary atresia, ventricular septal defect, and diminutive PAs by using a central end-to-side shunt. A total of 103 consecutive patients (71 male and 32 female) with pulmonary atresia, ventricular septal defect, and diminutive PAs received a central end-to-side shunt between PA and aorta from May 2004 to December 2010. The age and weight ranged between 2 to 86 months and 2.5 to 21.5 kg, respectively. Overall 79 patients with main PA diameters less than 4 mm received a central end-to-side shunt between PA and aorta, and 24 patients with main PAs absence received a modified central shunt between PA branches and aorta. There were no deaths during operation and follow-up. Compared with preoperative measures, total PA index increased from mean value 68.8 ± 11.4 mm2/m2 to 129.1 ± 24.9 mm2/m2 (p < 0.001). The increased PA index change at the time of 6 months or final repair after shunt completion was 87.7 ± 27.4% (27-150%). By multivariate regression analysis, age at shunt, shunt procedure, and number of major aortopulmonary collateral arteries were correlated with increasing PA index change. The central end-to-side shunt promoted sufficient growth of the diminutive central PAs, especially in infant patients. Due to the risk of a distortion of pulmonary branches, the authors interposed a modified procedure for patients with main PAs absence by anastomosis of left PA and right PA directly in an end-to-side fashion to the both lateral wall of ascending aorta. It is technically easy to perform, warrants low risk of shunt thrombosis, and flow restriction in the early postoperative period.
Publisher: Wiley
Date: 09-11-2016
DOI: 10.1111/JPI.12375
Abstract: Stress hyperglycemia is commonly observed in patients suffering from ischemic heart disease. It not only worsens cardiovascular prognosis but also attenuates the efficacies of various cardioprotective agents. This study aimed to investigate the protective effect of melatonin against myocardial ischemia-reperfusion (MI/R) injury in acute hyperglycemic state with a focus on Notch1/Hes1/Akt signaling and intracellular thioredoxin (Trx) system. Sprague Dawley rats were subjected to MI/R surgery and high-glucose (HG, 500 g/L) infusion (4 mL/kg/h) to induce temporary hyperglycemia. Rats were treated with or without melatonin (10 mg/kg/d) during the operation. Furthermore, HG (33 mmol/L)-incubated H9c2 cardiomyoblasts were treated in the presence or absence of luzindole (a competitive melatonin receptor antagonist), DAPT (a γ-secretase inhibitor), LY294002 (a PI3-kinase/Akt inhibitor), or thioredoxin-interacting protein (Txnip) adenoviral vectors. We found that acute hyperglycemia aggravated MI/R injury by suppressing Notch1/Hes1/Akt signaling and intracellular Trx activity. Melatonin treatment effectively ameliorated MI/R injury by reducing infarct size, myocardial apoptosis, and oxidative stress. Moreover, melatonin also markedly enhanced Notch1/Hes1/Akt signaling and rescued intracellular Trx system by upregulating Notch1, N1ICD, Hes1, and p-Akt expressions, increasing Trx activity, and downregulating Txnip expression. However, these effects were blunted by luzindole, DAPT, or LY294002. Additionally, Txnip overexpression not only decreased Trx activity, but also attenuated the cytoprotective effect of melatonin. We conclude that impaired Notch1 signaling aggravates MI/R injury in acute hyperglycemic state. Melatonin rescues Trx system by reducing Txnip expression via Notch1/Hes1/Akt signaling in a membrane receptor-dependent manner. Its role as a prophylactic/therapeutic drug deserves further clinical study.
Publisher: Springer Science and Business Media LLC
Date: 28-04-2017
DOI: 10.1007/S10495-017-1378-Y
Abstract: Diallyl trisulfide (DATS) protects against apoptosis during myocardial ischemia-reperfusion (MI/R) injury in diabetic state, although the underlying mechanisms remain poorly defined. Previously, we and others demonstrated that silent information regulator 1 (SIRT1) activation inhibited oxidative stress and endoplasmic reticulum (ER) stress during MI/R injury. We hypothesize that DATS reduces diabetic MI/R injury by activating SIRT1 signaling. Streptozotocin (STZ)-induced type 1 diabetic rats were subjected to MI/R surgery with or without perioperative administration of DATS (40 mg/kg). We found that DATS treatment markedly improved left ventricular systolic pressure and the first derivative of left ventricular pressure, reduced myocardial infarct size as well as serum creatine kinase and lactate dehydrogenase activities. Furthermore, the myocardial apoptosis was also suppressed by DATS as evidenced by reduced apoptotic index and cleaved caspase-3 expression. However, these effects were abolished by EX527 (the inhibitor of SIRT1 signaling, 5 mg/kg). We further found that DATS effectively upregulated SIRT1 expression and its nuclear distribution. Additionally, PERK/eIF2α/ATF4/CHOP-mediated ER stress-induced apoptosis was suppressed by DATS treatment. Moreover, DATS significantly activated Nrf-2/HO-1 antioxidant signaling pathway, thus reducing Nox-2/4 expressions. However, the ameliorative effects of DATS on oxidative stress and ER stress-mediated myocardial apoptosis were inhibited by EX527 administration. Taken together, these data suggest that perioperative DATS treatment effectively ameliorates MI/R injury in type 1 diabetic setting by enhancing cardiac SIRT1 signaling. SIRT1 activation not only upregulated Nrf-2/HO-1-mediated antioxidant signaling pathway but also suppressed PERK/eIF2α/ATF4/CHOP-mediated ER stress level, thus reducing myocardial apoptosis and eventually preserving cardiac function.
Publisher: Impact Journals, LLC
Date: 24-08-2017
Publisher: Hindawi Limited
Date: 08-01-2019
DOI: 10.1155/2019/7670854
Abstract: Endoplasmic reticulum (ER) stress and oxidative stress contribute greatly to myocardial ischemia-reperfusion (MI/R) injury. Naringenin, a flavonoid derived from the citrus genus, exerts cardioprotective effects. However, the effects of naringenin on ER stress as well as oxidative stress under MI/R condition and the detailed mechanisms remain poorly defined. This study investigated the protective effect of naringenin on MI/R-injured heart with a focus on cyclic guanosine monophosphate- (cGMP-) dependent protein kinase (PKG) signaling. Sprague-Dawley rats were treated with naringenin (50 mg/kg/d) and subjected to MI/R surgery with or without KT5823 (2 mg/kg, a selective inhibitor of PKG) cotreatment. Cellular experiment was conducted on H9c2 cardiomyoblasts subjected to simulated ischemia-reperfusion treatment. Before the treatment, the cells were incubated with naringenin (80 μ mol/L). PKGI α siRNA was employed to inhibit PKG signaling. Our in vivo and in vitro data showed that naringenin effectively improved heart function while it attenuated myocardial apoptosis and infarction. Furthermore, pretreatment with naringenin suppressed MI/R-induced oxidative stress as well as ER stress as evidenced by decreased superoxide generation, myocardial MDA level, gp91 phox expression, and phosphorylation of PERK, IRE1 α , and EIF2 α as well as reduced ATF6 and CHOP. Importantly, naringenin significantly activated myocardial cGMP-PKGI α signaling while inhibition of PKG signaling with KT5823 (in vivo) or siRNA (in vitro) not only abolished these actions but also blunted naringenin’s inhibitory effects against oxidative stress and ER stress. In summary, our study demonstrates that naringenin treatment protects against MI/R injury by reducing oxidative stress and ER stress via cGMP-PKGI α signaling. Its cardioprotective effect deserves further clinical study.
Location: China
Start Date: 2012
End Date: 2016
Funder: Major Military Project
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