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Objectives: To analyze the epidemiological characteristics and trends in death after thoracotomy in children with congenital heart disease (CHD). Methods: The clinical data of children with CHD aged 0–14 years who died after thoracotomy in our hospital from January 1, 2005, to December 31, 2020, were retrospectively collected to analyze the characteristics of and trends in postoperative death. Results: A total of 502 patients (365 males; 72.7%) died from January 1, 2005, to December 31, 2020, with an average of 31 deaths per year. For these patients, the median age was 2.0 months, the median length of hospital stay was 16.0 days, the median postoperative time to death was 5.0 days, and the median risk adjustment in congenital heart surgery-1 (RACHS-1) score was 3.0. 29.5% underwent emergency surgery, 16.9% had postoperative ECMO support, and 15.9% received postoperative blood purification treatment. In the past 16 years, the deaths of children with CHD under 1 year old accounted for 80.5% of all deaths among children with CHD aged 0–14 years, and deaths (349 cases) under 6 kg accounted for 69.5% of all deaths. Age at death, weight, and disease type were characterized by annual changes. Conclusions: The postoperative deaths of children with CHD mainly occurred in infants and toddlers who weighed less than 6.0 kg, and TGA and PA were the most lethal CHDs. The proportion of deaths has been increasing across the years among patients who are young, have a low body weight, and have complex cyanotic CHD. [ABSTRACT FROM AUTHOR]

Pulmonary stenosis (PS) is a congenital heart disease characterized by a dynamic or fixed anatomic obstruction of blood flow from the right ventricle to the pulmonary arterial vasculature. In the present study, extracellular vesicle long RNAs (EVLRs) from pregnant females who had healthy infants or PS infants were analyzed by RNA sequencing, and their diagnostic potential for PS during pregnancy was evaluated. A method for the selection of genes that could be considered as informative for the prediction PS based on extracellular vesicles (EVs) from pregnant females using long-read RNA sequencing was developed. Blood samples were collected from females carrying fetuses with PS and females carrying unaffected fetuses (n=6 in each group). Physical characterization of EVs was performed using nanoparticle tracking analysis, transmission electron microscopy and western blotting. EVLRs from plasma were profiled by RNA sequencing and mRNA co-expression modules were constructed by weighted gene co-expression network analysis (WGCNA). Gene Ontology (GO) enrichment analysis was used to predict the function of the genes in each module. Hub genes were filtered out based on WGCNA and visualized using Cytoscape. EVLRs consisted of mRNAs, microRNAs and long non-coding RNA. Overall, 26 modules were identified containing 16,394 genes. All modules were independent of each other. One particular module, referred to as the blue module, was markedly different between the two groups. A total of 735 hub genes in the blue module were identified, of which 33 were visualized, demonstrating the connection between these hub genes. GO enrichment analysis demonstrated that the analyzed hub genes were enriched in 'glucose transport', 'ATP-dependent chromatin remodeling', 'histone deacetylation', 'histone H3-K4 methylation', 'DNA methylation', 'apoptotic signaling pathway' and 'glucocorticoid receptor signaling pathway'. The hub genes identified in this module may provide a genetic framework for prenatal PS diagnosis. Furthermore, functional analysis of these associated genes may provide a theoretical basis for further research on PS pathogenesis. [ABSTRACT FROM AUTHOR]

Background: Certain pregnant women suffer from cardiac pathology,and a few of them need cardiac operations under cardiopulmonary bypass during pregnancy. Feto-neonatal and maternal outcomes have not been sufficiently described.Methods: We conducted a retrospective review of 22 cases of women undergoing cardiac operations under cardiopulmonary bypass during pregnancy in our hospital from Jan.2014 to Mar.2019.Results: All 22 patients were alive after treatment. The types of cardiac disorders included congenital heart defects, rheumatic heart disease,infective endocarditis,aortic dissection, obstruction and/or thrombosis of a prosthetic valve. Only one case was a twin pregnancy,and the other 21 cases were singletons. Four fetuses died in the utero after surgery. Three patients chose termination of the pregnancy after the cardiac operations: one fetus was detected abnormity of the brain and the other two patients abandoned pregnancy. Fourteen fetuses were alive and born without any abnormity. Two fetuses suffered from neonatal intracranial hemorrhage and died after birth.Conclusions: Cardiac operation under cardiopulmonary bypass during pregnancy is a challenge for physicians in multidisciplinary teams. Strictly evaluating the indication is vital. On the other hand, some patients can benefit from this management. [ABSTRACT FROM AUTHOR]

Perfluorooctane sulfonate (PFOS), an endocrine-disrupting chemical pollutant, affects embryonic heart development; however, the mechanisms underlying its toxicity have not been fully elucidated. Here, Single-cell RNA sequencing (scRNA-seq) was used to investigate the overall effects of PFOS on myocardial differentiation from human embryonic stem cells (hESCs). Additionally, apoptosis, mitochondrial membrane potential, and ATP assays were performed. Downregulated cardiogenesis-related genes and inhibited cardiac differentiation were observed after PFOS exposure in vitro. The percentages of cardiomyocyte and cardiac progenitor cell clusters decreased significantly following exposure to PFOS, while the proportion of primitive endoderm cell was increased in PFOS group. Moreover, PFOS inhibited myocardial differentiation and blocked cellular development at the early- and middle-stage. A Gene Ontology analysis and pseudo-time trajectory illustrated that PFOS disturbed multiple processes related to cardiogenesis and oxidative phosphorylation in the mitochondria. Furthermore, PFOS decreased mitochondrial membrane potential and induced apoptosis. These results offer meaningful insights into the cardiogenic toxicity of PFOS exposure during heart formation as well as the adverse effects of PFOS on mitochondria. [Display omitted] • Sc-RNA sequencing displayed the transcriptional dynamics of cardiomyocytes differentiation during PFOS exposure. • PFOS produced the decrease of hESC differentiation into cardiac progenitor cell but increase of primitive endoderm cell. • PFOS interfered myocardial differentiation by blocking cells at earlier stage. • PFOS decreased mitochondria membrane potential and induced cells apoptosis. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the influence and possible pathophysiological mechanism of pulsatile cardiopulmonary bypass (CPB) in various frequencies in pediatric patients undergoing congenital cardiac surgery.Patients and Methods: Clinical data and hemodynamic parameters were collected in 80 patients who underwent congenital cardiac surgeries and were perfused in different settings: pulsatile perfusion (PP) in frequencies of 30 beats/min, PP 60 beats/min, PP 100 beats/min and non-pulsatile perfusion (NP). Serum proteins, plasma-free hemoglobin (PFH), endothelin-1 (ET-1) and nitric oxide (NO) were collected to study possible pathophysiological changes, possible hematological injury and oxidative status under different perfusing conditions.Results: Patients in all groups had similar baseline characteristics, aortic cross-clamping time and CPB duration. More effective pulse gradient (PG), energy-equivalent pressure (EEP) and surplus hemodynamic energy (SHE) were observed in pulsatility with lower frequency setting, under which more patients achieved physiologically normal mean arterial pressure (MAP), without the support of inotropic agents during bypass. Significant between-group differences of serum proteins and PFH were absent the whole time during and after bypass, while a relatively lower percentage of perioperative requirement of diuretics was observed in the low frequency pulsatile group. A better performance to oxidative stress was seen in the low frequency group with higher levels of NO and lower concentration of ET-1, and both intergroup differences were found (P<0.01). Satisfactory clinical outcome was obtained on post procedure course in all groups.Conclusion: Pulsatile perfusion with low frequency setting in pediatric patients undergoing congenital cardiac surgery showed better hemodynamic profiles, potential protective effects on vital organs, better oxidative status and satisfactory clinical outcome. [ABSTRACT FROM AUTHOR]

Tobacco smoking was one of the important adverse factors for congenital heart disease. The effects of nicotine, the main component of tobacco, on human embryonic cardiogenesis and related mechanisms remain poorly understood. This work used single-cell RNA sequencing to investigate the effects of nicotine on human embryonic stem cell (hESC) line H9 and its underlying mechanisms during cardiac differentiation. H9 was cultured in feeder-free medium and differentiated in cardiac condition medium when cells reached 90% confluent. Cell viability was detected by MTT after different concentration of nicotine treatment. Different expressed genes during cardiac differentiation was analyzed by single-cell RNA sequencing (scRNA-seq). Key gene expressions were confirmed by qPCR and Western blot. Results showed that 0.1μM–10μM nicotine did not affect H9 cell proliferation. Nicotine 1 μM down-regulated cardiac progenitor cell, mesoderm cell, smooth muscle cell and neural crest cell relatively. Snail1/2 regulating endocardial cushion development were downregulated apparently at differention day 6. Nicotine didn't affect bry-1 and mesp-1 but inhibited cardiac transcript factors. Consequently, the expression of cTnI, a marker of cardiomyocytes was decreased significantly. The data suggest direct adverse effects of nicotine on heart development at the single-cell level and offer a new approach for estimate drug and environmental toxicity on the pathogenesis of the embryonic cardiovascular system development. • Nicotine affected cardiac differentiation from hESCs. • Dataset of scRNA-seq was valuable for estimate nicotine toxicity. [ABSTRACT FROM AUTHOR]