Advancing cardiac regeneration through 3D bioprinting: methods, applications, and future directions.

Cardiovascular diseases (CVDs) represent a paramount global mortality concern, and their prevalence is on a relentless ascent. Despite the effectiveness of contemporary medical interventions in mitigating CVD-related fatality rates and complications, their efficacy remains curtailed by an array of limitations. These include the suboptimal efficiency of direct cell injection and an inherent disequilibrium between the demand and availability of heart transplantations. Consequently, the imperative to formulate innovative strategies for cardiac regeneration therapy becomes unmistakable. Within this context, 3D bioprinting technology emerges as a vanguard contender, occupying a pivotal niche in the realm of tissue engineering and regenerative medicine. This state-of-the-art methodology holds the potential to fabricate intricate heart tissues endowed with multifaceted structures and functionalities, thereby engendering substantial promise. By harnessing the prowess of 3D bioprinting, it becomes plausible to synthesize functional cardiac architectures seamlessly enmeshed with the host tissue, affording a viable avenue for the restitution of infarcted domains and, by extension, mitigating the onerous yoke of CVDs. In this review, we encapsulate the myriad applications of 3D bioprinting technology in the domain of heart tissue regeneration. Furthermore, we usher in the latest advancements in printing methodologies and bioinks, culminating in an exploration of the extant challenges and the vista of possibilities inherent to a diverse array of approaches.

Genetic analysis of potential biomarkers and therapeutic targets in ferroptosis from coronary artery disease.

Ferroptosis plays a key role in the death of cells including cardiomyocytes, and it is related to a variety of cardiac diseases. However, the role of ferroptosis-related genes (FRGs) in coronary artery disease (CAD) is not well characterized. We downloaded CAD-related information and FRGs from the gene expression omnibus (GEO) database and Ferroptosis Database (FerrDb) respectively. A total of 10 CAD-related DE-FRGs were obtained, which were closely linked to autophagy regulation and immune response. Subsequently, CA9, CBS, CEBPG, HSPB1, SLC1A4, STMN1 and TRIB3 among the 10 DE-FRGs were identified as marker genes by LASSO and SVM-RFE algorithms, which had tolerable diagnostic capabilities. Subsequent functional enrichment analysis showed that these marker genes may play a corresponding role in CAD by participating in the regulation of immune response, amino acid metabolism, cell cycle and multiple pathways related to the pathogenesis of CAD. Furthermore, a total of 58 drugs targeting 7 marker genes had been obtained. On the contrary, the ceRNA network revealed a complex regulatory relationship based on the marker genes. Also, CIBERSORT analysis showed that the changes in the immune microenvironment of CAD patients may be related to CBS, HSPB1 and CEBPG. We developed a diagnostic potency and provided an insight for exploring the mechanism for CAD. Before clinical application, further research is needed to test its diagnostic value for CAD.

Exosomes in atrial fibrillation: therapeutic potential and role as clinical biomarkers.

Atrial fibrillation (AF), the most common cardiac arrhythmia, is a global epidemic. AF can cause heart failure and myocardial infarction and increase the risk of stroke, disability, and thromboembolic events. AF is becoming increasingly ubiquitous and is associated with increased morbidity and mortality at higher ages, resulting in an increasing threat to human health as well as substantial medical and social costs. Currently, treatment strategies for AF focus on controlling heart rate and rhythm with medications to restore and maintain sinus rhythm, but this approach has limitations. Catheter ablation is not entirely satisfactory and does not address the issues underlying AF. Research exploring the mechanisms causing AF is urgently needed for improved prevention, diagnosis, and treatment of AF. Exosomes are small vesicles (30-150 nm) released by cells that transmit information between cells. MicroRNAs in exosomes play an important role in the pathogenesis of AF and are established as a biomarker for AF. In this review, a summary of the role of exosomes in AF is presented. The role of exosomes and microRNAs in AF occurrence, their therapeutic potential, and their potential role as clinical biomarkers is considered. A better understanding of exosomes has the potential to improve the prognosis of AF patients worldwide, reducing the global medical burden of this disease.

Individualized right ventricular outflow tract reconstruction using autologous pulmonary tissue in situ for the treatment of pulmonary atresia with ventricular septum defect.

OBJECTIVE: The study aims to evaluate the feasibility and effectiveness of an individualized procedure for right ventricular outflow tract (RVOT) reconstruction in pulmonary atresia with ventricular septal defect (PA-VSD). METHODS: RVOT was reconstructed using autologous pulmonary artery tissue preserved in situ as the posterior wall and a bovine jugular vein patch (BJVP) as the anterior wall in patients with PA-VSD (observation group). The size of the BJVP made from a bovine jugular vein conduit (BJVC) was individually calculated using a formula based on the child's weight and the size of the autologous pulmonary artery (the diameter of BJVC DB⁢J⁢V⁢C = Dt⁢h⁢e⁢o⁢r⁢e⁢t⁢i⁢c⁢a⁢l-W⁢z^-4π). Its effect was then compared with the conventional modified Rastelli procedure based on the BJVC (control group). RESULTS: A total of 22 patients that underwent the new procedure were simultaneously compared with the 25 patients in the control group. No deaths occurred in both groups. Notably, there were no significant differences in mechanical ventilation, ICU and postoperative residence, cardiopulmonary bypass, and aortic cross-clamp time. In the follow-up, which spanned for 8-12 years (mean 9.2 years), only four cases with moderate regurgitation were noted in the observation group without obstruction. In the control group, two patients had a conduit replacement. Three patients suffered from anastomotic stenosis, which was corrected by balloon dilatation. CONCLUSION: Individualized RVOT reconstruction with autologous pulmonary tissue preserved in situ as the posterior wall is adequate for treating PA-VSD.

Risk factors for venoarterial-extracorporeal membrane oxygenation related nosocomial infection in children after cardiac surgery. / 儿童心脏术后静脉-åŠ¨è„‰ä½“å¤–è†œè‚ºæ°§åˆç›¸å ³åŒ»é™¢å† æ„ŸæŸ“çš„å±é™©å› ç´ .

OBJECTIVES: Extracorporeal membrane oxygenation (ECMO) is an extracorporeal life support strategy for the treatment of critically ill children with reversible heart and lung failure, increasingly being used in patients with low cardiac output after cardiac surgery. However, the mortality of patients is closely related to the complications of ECMO, especially bleeding, thrombosis, and infection, ECMO-related nosocomial infection has become a challenge to the success of ECMO. This study aims to analyze the incidence and risk factors for venoarterial-ECMO (VA-ECMO)-related nosocomial infections in children after cardiac surgery. METHODS: We retrospectively collected the data of patients who underwent VA-ECMO treatment after pediatric cardiac surgery in the Second Xiangya Hospital of Central South University from July 2015 to March 2021, and divided them into an infected group and a non-infected group. The clinical characteristics of the 2 groups of patients, VA-ECMO-related nosocomial infection factors, pathogenic microorganisms, and patient mortality were compared. Logistic regression was used to analyze the risk factors for nosocomial infection related to VA-ECMO after cardiac surgery. RESULTS: Of the 38 pediatric patients, 18 patients (47.37%) had VA-ECMO related nosocomial infection, served as the infected group, including 7 patients with blood infections and 11 respiratory tract infections. Gram-negative pathogens (16 strains, 88.9%) were the main bacteria, such as Acinetobacter baumannii (6 strains), Klebsiella pneumoniae (3 strains), and Stenotrophomonas maltophilia (3 strains). Compared with the non-infected group (n=20), the infection group had longer time of cardiopulmonary bypass, time of myocardial block, and time of VA-ECMO assistance (All P<0.05). Multivariate logistic regression analysis showed that time of cardiopulmonary bypass (OR=1.012, 95% CI 1.002 to 1.022; P=0.021) was an independent risk factor for ECMO-related nosocomial infection. The number of surviving discharges in the infected group was less than that in the non-infected group (1 vs 11, P<0.05). CONCLUSIONS: Cardiopulmonary bypass time is an independent risk factor for VA-ECMO-related nosocomial infection in children after cardiac surgery. Shortening the duration of extracorporeal circulation may reduce the incidence of VA-EMCO-related nosocomial infections in children after cardic surgery. The occurrence of VA-ECMO-related nosocomial infections affects the number of patient's discharge alive.

RIP1/RIP3/MLKL-mediated necroptosis contributes to vinblastine-induced myocardial damage.

Vinblastine (VBL) has been considered as a first-line anti-tumor drug for many years. However, vinblastine-caused myocardial damage has been continually reported. The underlying molecular mechanism of the myocardial damage remains unknown. Here, we show that vinblastine induces myocardial damage and necroptosis is involved in the vinblastine-induced myocardial damage both in vitro and in vivo. The results of WST-8 and flow cytometry analysis show that vinblastine causes damage to H9c2 cells, and the results of animal experiments show that vinblastine causes myocardial cell damage. The necrosome components, receptor-interacting protein 1 (RIP1) receptor-interacting protein 3 (RIP3), are significantly increased in vinblastine-treated H9c2 cells, primary neonatal rat ventricular myocytes and rat heart tissues. And the downstream substrate of RIP3, mixed lineage kinase domain like protein (MLKL) was also increased. Pre-treatment with necroptosis inhibitors partially inhibits the necrosome components and MLKL levels and alleviates vinblastine-induced myocardial injury both in vitro and in vivo. This study indicates that necroptosis participated in vinblastine-evoked myocardial cell death partially, which would be a potential target for relieving the chemotherapy-related myocardial damage.

Cardiomyocytes from CCND2-overexpressing human induced-pluripotent stem cells repopulate the myocardial scar in mice: A 6-month study.

BACKGROUND: Cardiomyocytes that have been differentiated from CCND2-overexpressing human induced-pluripotent stem cells (hiPSC-CCND2OE CMs) can proliferate when transplanted into mouse hearts after myocardial infarction (MI). However, it is unknown whether remuscularization can replace the thin LV scar and if the large muscle graft can electrophysiologically synchronize to the recipient myocardium. Our objectives are to evaluate the structural and functional potential of hiPSC-CCND2OE CMs in replacing the LV thin scar. METHODS: NOD/SCID mice were treated with hiPSC-CCND2OE CMs (i.e., the CCND2OE group), hiPSC-CCND2WT CMs (the CCND2WT group), or an equal volume of PBS immediately after experimentally-induced myocardial infarction. The treatments were administered to one site in the infarcted zone (IZ), two sites in the border zone (BZ), and a fourth group of animals underwent Sham surgery. RESULTS: Six months later, engrafted cells occupied >50% of the scarred region in CCND2OE animals, and exceeded the number of engrafted cells in CCND2WT animals by ~8-fold. Engrafted cells were also more common in the IZ than in the BZ for both cell-treatment groups. Measurements of cardiac function, infarct size, wall thickness, and cardiomyocyte hypertrophy were significantly improved in CCND2OE animals compared to animals from the CCND2WT or PBS-treatment groups. Measurements in the CCND2WT and PBS groups were similar, and markers for cell cycle activation and proliferation were significantly higher in hiPSC-CCND2OE CMs than in hiPSC-CCND2WT CMs. Optical mapping of action potential propagation indicated that the engrafted hiPSC-CCND2OE CMs were electrically coupled to each other and to the cells of the native myocardium. No evidence of tumor formation was observed in any animals. CONCLUSIONS: Six months after the transplantation, CCND2-overexpressing hiPSC-CMs proliferated and replaced >50% of the myocardial scar tissue. The large graft hiPSC-CCND2OE CMs also electrically integrated with the host myocardium, which was accompanied by a significant improvement in LV function.

Magnesium Lithospermate B Derived from Salvia miltiorrhiza Ameliorates Right Ventricle Remodeling in Pulmonary Hypertensive Rats via Inhibition of NOX/VPO1 Pathway.

Right ventricle (RV) remodeling is a major pathological feature in pulmonary arterial hypertension (PAH). Magnesium lithospermate B (MLB) is a compound isolated from the roots of Salvia miltiorrhiza and it possesses multiple pharmacological activities such as anti-inflammation and antioxidation. This study aims to investigate whether MLB is able to prevent RV remodeling in PAH and the underlying mechanisms. In vivo, SD rats were exposed to 10% O2 for 21 d to induce RV remodeling, which showed hypertrophic features (increases in the ratio of RV weight to tibia length, cellular size, and hypertrophic marker expression), accompanied by upregulation in expression of NADPH oxidases (NOX2 and NOX4) and vascular peroxidase 1 (VPO1), increases in hydrogen peroxide (H2O2) and hypochlorous acid (HOCl) production and elevation in phosphorylation levels of ERK; these changes were attenuated by treating rats with MLB. In vitro, the cultured H9c2 cells were exposed to 3% O2 for 24 h to induce hypertrophy, which showed hypertrophic features (increases in cellular size and hypertrophic marker expression). Administration of MLB or VAS2870 (a positive control for NOX inhibitor) could prevent cardiomyocyte hypertrophy concomitant with decreases in NOX (NOX2 and NOX4) and VPO1 expression, H2O2 and HOCl production, and ERK phosphorylation. Based on these observations, we conclude that MLB is able to prevent RV remodeling in hypoxic PAH rats through a mechanism involving a suppression of NOX/VPO1 pathway as well as ERK signaling pathway. MLB may possess the potential clinical value for PAH therapy.

Reabsorbable Pins can Reinforce an Early Sternal Stability After Median Sternotomy in Young Children with Congenital Heart Disease.

We evaluated the efficacy of bioresorbable sternal reinforcement device (poly-L-lactide sternal pins) on sternal healing after median sternotomy in young children (with body weight less than 10 kg) with congenital heart disease (CHD). Data from 85 patients, who underwent CHD surgery through median sternotomy from October 2016 to May 2018, were collected and analyzed. Sternal pins were utilized in 85 patients (10 mm × 1 mm × 1 mm for patients with body weights less than 5 kg and 15 mm × 2 mm × 2 mm for those weighing between 5 and 10 kg) in addition to sternum closure with Ethicon PDSTMII running sutures (Group A), while 84 patients received the Ethicon sternal closure (Group B) with no pins. The occurrence of sternal dehiscence, anterior-posterior displacement, and high-low displacement was evaluated by physical examination and three-dimensional computed tomography at one month postoperatively. No anterior-posterior sternal displacement (0%) was observed in Group A, while 10 anterior-posterior displacements (11.9%) were observed in Group B (P < 0.01). The number of sternal caudal-cranial displacements in Groups A and B was 4 (4.71%) and 5 (5.35%), respectively (P = 0.870). While no sternal dehiscence (0%) was observed in Group A, 7 out of 84 patients (8.33%) in Group B exhibited obvious sternal dehiscence (P < 0.01). The bioresorbable poly-L-lactide sternal pins reduced an anterior-posterior sternal displacement and sternal dehiscence, which was accompanied by a significant improvement of an early sternal fixation.

[Application of the index system for clinical evaluation of implementation effect: An example of vaginal delivery].

OBJECTIVE: In order to apply the index system for clinical evaluation of implementation effect in hospitals.
 Methods: A total of 862 patients with vaginal delivery from 9 hospitals were randomly divided into an clinical pathway group (n=496) and a control group (n=366). The patients in the control group received traditional treatment procedure while the patients in the clinical pathway group experienced procedure of the clinical treatment. The index system was used for clinical evaluation of implementation effect.
 Results: There were obvious advantages in 15 indicators in the clinical pathway group than those in the control group (P<0.05). The comprehensive score of the clinical pathway group was higher than the control group of the corresponding grade and nature of the hospital. The comprehensive score for secondary hospitals (Ci=0.7967) were higher than that for the tertiary hospitals (Ci=0.2033). The comprehensive score for the general hospitals (Ci=0.8948) were higher than that for the specialized hospitals (Ci=0.1052). As for clinical implementation effect, the secondary hospitals were better than the tertiary hospital, and the general hospitals were better than the specialized hospitals.
 Conclusion: The index system for clinical evaluation could quantify the implementation effect, and compare the implementation effect in different hospitals, which provides reference for the management of clinical pathway.

Suppression of NADPH oxidase attenuates hypoxia-induced dysfunctions of endothelial progenitor cells.

NADPH oxidases (NOX) - derived reactive oxygen species (ROS) contribute to oxidative injury in hypoxia-induced pulmonary arterial hypertension. This study aims to evaluate the status of NOX in endothelial progenitor cells (EPCs) under hypoxic condition and to determine whether NOX inhibitors could attenuate hypoxia-induced dysfunctions of EPCs. EPCs were isolated from peripheral blood of SD rats and subjected to hypoxia (O2/N2/CO2, 1/94/5) for 24 h. The cells were collected for ß-galactosidase or Hoechst staining, or for functional analysis (migration, adhesion and tube formation). The NOX expression, activity and H2O2 content in EPCs were measured. The results showed that hypoxia treatment promoted EPC senescence and apoptosis, accompanied by the deteriorated functions of EPCs (the reduced abilities in adhesion, migration and tube formation), as well as an increase in NOX2 and NOX4 expression, NOX activity and H2O2 production, these phenomena were attenuated by NOX inhibitors. Furthermore, administration of catalase could also improve the functions of hypoxia-treated EPCs. Based on these observations, we conclude that NOX-derived ROS contributes to the dysfunctions of EPCs under hypoxic condition. Thus, suppression of NOX may provide a novel strategy to improve endothelial functions in hypoxia-relevant diseases.

A rare, giant coronary artery ectasia coexisting with a coronary artery fistula in an older infant.

Coronary artery fistula with giant coronary artery ectasia is a rare abnormal CHD. Multidetector CT is useful for the diagnosis. Early diagnosis and surgery are recommended.

Initial Research on Postoperative Management of Tetralogy of Fallot with Major Aortopulmonary Collaterals.

OBJECTIVES: Tetralogy of Fallot (TOF) with major aortopulmonary collaterals (MAPCA) is a well-known but always severe congenital heart disease. This study was designed to explore proper management after radical correction of TOF with MAPCA based on a hierarchical approach. METHODS: The following data were collected from 39 patients planned to undergo radical correction of TOF: age, weight, number of aortopulmonary collaterals, total lumen diameter and collateral diameter-to-body weight ratio, transcatheter occlusion and cardiac catheterization findings, mechanical ventilation time, and ICU monitoring time. The patients were divided into 4 groups by collateral diameter-to-body weight ratio as follows: <0.200 mm/kg (group 1), 0.200-0.500 mm/kg (group 2), >0.500 mm/kg (group 3), and no MAPCA (group 4). Data analysis was performed using IBM SPSS Statistics software for Mac version 22.0 (SPSS Inc., Chicago, Ill., USA) with logistic regression and Fisher's exact test. RESULTS: Most of the patients recovered well after radical correction; postoperative complications occurred in 12 patients and included bloody sputum, low cardiac output syndrome, and severe pulmonary infection that led to tracheotomy. By prolonging the mechanical ventilation time of the patients with postoperative complications, the conditions in 3 patients were improved. However, in the remaining patients, the condition worsened until transcatheter occlusions were performed. Transcatheter occlusion was performed in all 7 patients in group 3 (100%). Only 2 of the 8 patients in group 2 required transcatheter occlusion (25%), and none of the 9 patients in group 1 required transcatheter occlusion (0%). Only 1 patient (group 3) died after radical correction. The transcatheter occlusion results showed a strong association with the total lumen diameter and the collateral diameter-to-body weight ratio (p < 0.05) but no obvious association with age, weight, or the number of aortopulmonary collaterals (p > 0.05). CONCLUSIONS: Postoperative management of patients with TOF and MAPCA has great significance. To reduce the morbidity and mortality, transcatheter coil embolization or surgical ligation should be performed in patients with a collateral diameter-to-body weight ratio of at least 0.500 mm/kg. In patients with values between approximately 0.200 and 0.500 mm/kg, prolongation of mechanical ventilation should have priority over transcatheter occlusion, and for patients with values below 0.200 mm/kg no additional treatment is needed.

[Hybrid procedure for infants/children treatment with pulmonary stenosis under transesophageal echocardiographic guidance].

OBJECTIVE: To investigate the outcomes of hybrid procedure in treating 10 infants/children with pulmonary stenosis under transesophageal echocardiographic guidance.
 METHODS: Between September, 2009 and December, 2015, 10 infants/children underwent hybrid procedure of transthoracic balloon pulmonary valvuloplasty for pulmonary stenosis in the Second Xiangya Hospital, Central South University. The age, height and weight at the time of admission were 0.7-42 (14.8±15.8) months, 53-97 (74.8±16.3) cm, and 4-15.5 (9.3±4.1) kg, respectively. Atrial septal defect, patent foramen ovale, patent ductus arteriosus, muscular ventricular septal defect, persistent left superior vena cava and tricuspid regurgitation were found in 2, 6, 1, 2, 1 and 5 cases, respectively.
 RESULTS: After the operation, all patients were sent into ICU. The mean duration mechanical ventilation, ICU stay and hospitalization were 0.5-41(6.8±12.3) h, 2-85 (31.1±22.8) h, and 6-20 (11.4±5.1) d, respectively. Postoperative transvalvular pressure gradient reduced to 16-45 (31.1±9.8) mmHg, which was decreased significantly compared with that in preoperative (P<0.001). There was no death during hospitalization and follow-up.
 CONCLUSION: Hybrid procedure of transthoracic balloon pulmonary valvuloplasty for pulmonary stenosis under transesophageal echocardiographic guidance is a safe and effective treatment.

Duplication of 10q22.3-q23.3 encompassing BMPR1A and NGR3 associated with congenital heart disease, microcephaly, and mild intellectual disability.

Chromosome region 10q22.3-q23.3 contains several low copy repeats (LCRs) and is prone to recombination. Deletions with breakpoints within LCR3 and LCR4 have been described to be associated with intellectual disability and dysmorphic features, while the reciprocal duplications are rarely reported. We present an additional case with multiple congenital anomalies that include microcephaly, cardiac defect, and mild intellectual disability, in which a de novo interstitial 8.2-Mb duplication of 10q22.3-q23.3, including BMPR1A and NGR3, was identified by Illumina SNP array platform. Our study is consistent with the hypothesis that the BMPR1A is a plausible candidate gene for congenital heart disease (CHD) and should contribute to the diagnosis and treatment of these genomic diseases.

Effect of social support and coping styles on the stress and mental health in relatives of patients with traumatic brain injury.

OBJECTIVE: To investigate the effect of social support and coping style on the stress and mental health in relatives of patients with traumatic brain injury. METHODS: The stress, mental health, social support and coping style were investigated in 300 relatives of patients with traumatic brain injury by Relative Stress Scale, Symptom Checklist-90, Social Support Rating Scale and Simplified Coping Style Questionnaire in Changsha City. RESULTS: The mental health problems in relatives of patients with traumatic brain injury were closely related to the levels of stress, the ways of coping and the social support. In addition to the direct eff ect of stress on mental health in relatives of patients, the ways of coping and social support functioned as a mediator in this regard. The value of mesomeric eff ect for coping styles and social support ranged from 23.6% to 43.0%, and social support had an advantage over the coping styles. CONCLUSION: Social support and coping styles should be considered in psychological nursing program to prevent and adjust the mental distress in relatives of patients with traumatic brain injury, which is beneficial to the treatment and recovery for patients.

Regulation of Mcl-1 by constitutive activation of NF-κB contributes to cell viability in human esophageal squamous cell carcinoma cells.

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is one of the most lethal malignancies with a 5-year survival rate less than 15%. Understanding of the molecular mechanisms involved in the pathogenesis of ESCC becomes critical to develop more effective treatments. METHODS: Mcl-1 expression was measured by reverse transcription (RT)-PCR and Western blotting. Human Mcl-1 promoter activity was evaluated by reporter gene assay. The interactions between DNA and transcription factors were confirmed by electrophoretic mobility shift assay (EMSA) in vitro and by chromatin immunoprecipitation (ChIP) assay in cells. RESULTS: Four human ESCC cell lines, TE-1, Eca109, KYSE150 and KYSE510, are revealed increased levels of Mcl-1 mRNA and protein compare with HaCaT, an immortal non-tumorigenic cell line. Results of reporter gene assays demonstrate that human Mcl-1 promoter activity is decreased by mutation of kappaB binding site, specific NF-kappaB inhibitor Bay11-7082 or dominant inhibitory molecule DNMIkappaBalpha in TE-1 and KYSE150 cell lines. Mcl-1 protein level is also attenuated by Bay11-7082 treatment or co-transfection of DNMIkappaBalpha in TE-1 and KYSE150 cells. EMSA results indicate that NF-kappaB subunits p50 and p65 bind to human Mcl-1-kappaB probe in vitro. ChIP assay further confirm p50 and p65 directly bind to human Mcl-1 promoter in intact cells, by which regulates Mcl-1 expression and contributes to the viability of TE-1 cells. CONCLUSIONS: Our data provided evidence that one of the mechanisms of Mcl-1 expression in human ESCC is regulated by the activation of NF-kappaB signaling. The newly identified mechanism might provide a scientific basis for developing effective approaches to treatment human ESCC.

A minimally invasive technique for occluding large muscular ventricular septal defects in infants.

OBJECTIVE: This study investigated the feasibility, timing and indications for closure of large muscular ventricular septal defects (VSDs) in infants without use of a cardiopulmonary bypass. METHODS: A total of 9 infants with large muscular VSDs ranging in size from 7 to 15 mm were treated by minimally invasive closure without cardiopulmonary bypass between April 2010 and February 2013. RESULTS: All surgeries were successful without resulting in uncontrolled systemic infection, a pulmonary hypertensive crisis or a severely low cardiac output, and with an apparently shorter operation time and postoperative tracheal cannula. CONCLUSIONS: VSD closure without cardiopulmonary bypass can improve the efficacy and prognosis of infants with large muscular VSDs and concurrent pulmonary infections or respiratory failure.

Echocardiographic assessment and guidance in minimally invasive surgical device closure of perimembranous ventricular septal defects.

BACKGROUND: The primary aim of this study was to explore the safety and feasibility of minimally invasive surgical device closure of perimembranous ventricular septal defects (PMVSDs) in children using echocardiography for preoperative assessment and intraoperative guidance. METHODS: We enrolled 942 children diagnosed with PMVSDs from April 2010 to October 2013. All children underwent full evaluation by transthoracic echocardiography (TTE) and multiplane transesophageal echocardiography (MTEE) to determine the sizes, types and spatial positions of defects and their proximity to the adjacent tissues. The PMVSDs were surgically occluded using MTEE for guidance. RESULTS: Eight hundred eighty-nine (94.37%) of 942 children underwent successful closure of PMVSDs. Symmetric devices were used in 741 children (including 38 A4B2 occluders) and asymmetric devices were used in the other 148. All patients received follow-ups at regular intervals after successful occlusion. The occluders remained firmly in place. No noticeable residual shunt or valvular regurgitation was discovered, with the exception of one child whose original mild aortic regurgitation progressed to moderate by the 18 month follow-up. Overall there were no significant arrhythmias with the exception of 3 children, all of whom experienced postsurgical acute attacks of Adams-Stokes syndrome. CONCLUSIONS: Minimally invasive surgical device closure of PMVSDs is safe and feasible. TTE and MTEE play vital roles in all stages of treatment of PMVSDs.