Optimization and evaluation of facial recognition models for Williams-Beuren syndrome.

Williams-Beuren syndrome (WBS) is a rare genetic disorder characterized by special facial gestalt, delayed development, and supravalvular aortic stenosis or/and stenosis of the branches of the pulmonary artery. We aim to develop and optimize accurate models of facial recognition to assist in the diagnosis of WBS, and to evaluate their effectiveness by using both five-fold cross-validation and an external test set. We used a total of 954 images from 135 patients with WBS, 124 patients suffering from other genetic disorders, and 183 healthy children. The training set comprised 852 images of 104 WBS cases, 91 cases of other genetic disorders, and 145 healthy children from September 2017 to December 2021 at the Guangdong Provincial People's Hospital. We constructed six binary classification models of facial recognition for WBS by using EfficientNet-b3, ResNet-50, VGG-16, VGG-16BN, VGG-19, and VGG-19BN. Transfer learning was used to pre-train the models, and each model was modified with a variable cosine learning rate. Each model was first evaluated by using five-fold cross-validation and then assessed on the external test set. The latter contained 102 images of 31 children suffering from WBS, 33 children with other genetic disorders, and 38 healthy children. To compare the capabilities of these models of recognition with those of human experts in terms of identifying cases of WBS, we recruited two pediatricians, a pediatric cardiologist, and a pediatric geneticist to identify the WBS patients based solely on their facial images. We constructed six models of facial recognition for diagnosing WBS using EfficientNet-b3, ResNet-50, VGG-16, VGG-16BN, VGG-19, and VGG-19BN. The model based on VGG-19BN achieved the best performance in terms of five-fold cross-validation, with an accuracy of 93.74% ± 3.18%, precision of 94.93% ± 4.53%, specificity of 96.10% ± 4.30%, and F1 score of 91.65% ± 4.28%, while the VGG-16BN model achieved the highest recall value of 91.63% ± 5.96%. The VGG-19BN model also achieved the best performance on the external test set, with an accuracy of 95.10%, precision of 100%, recall of 83.87%, specificity of 93.42%, and F1 score of 91.23%. The best performance by human experts on the external test set yielded values of accuracy, precision, recall, specificity, and F1 scores of 77.45%, 60.53%, 77.42%, 83.10%, and 66.67%, respectively. The F1 score of each human expert was lower than those of the EfficientNet-b3 (84.21%), ResNet-50 (74.51%), VGG-16 (85.71%), VGG-16BN (85.71%), VGG-19 (83.02%), and VGG-19BN (91.23%) models. CONCLUSION: The results showed that facial recognition technology can be used to accurately diagnose patients with WBS. Facial recognition models based on VGG-19BN can play a crucial role in its clinical diagnosis. Their performance can be improved by expanding the size of the training dataset, optimizing the CNN architectures applied, and modifying them with a variable cosine learning rate. WHAT IS KNOWN: • The facial gestalt of WBS, often described as "elfin," includes a broad forehead, periorbital puffiness, a flat nasal bridge, full cheeks, and a small chin. • Recent studies have demonstrated the potential of deep convolutional neural networks for facial recognition as a diagnostic tool for WBS. WHAT IS NEW: • This study develops six models of facial recognition, EfficientNet-b3, ResNet-50, VGG-16, VGG-16BN, VGG-19, and VGG-19BN, to improve WBS diagnosis. • The VGG-19BN model achieved the best performance, with an accuracy of 95.10% and specificity of 93.42%. The facial recognition model based on VGG-19BN can play a crucial role in the clinical diagnosis of WBS.

AmCBF1 activates the expression of GhClpR1 to mediate dark-green leaves in cotton (Gossypium hirsutum).

KEY MESSAGE: The transcription factor AmCBF1 deepens the leaf colour of transgenic cotton by binding to the promoter of the chloroplast development-related protein GhClpR1 to promote photosynthesis. The ATP-dependent caseinolytic protease (Clp protease) family plays a crucial role within chloroplasts, comprising several Clp proteins to maintain chloroplast homeostasis. At present, research on Clp proteins mainly focuses on Arabidopsis, leaving its function in other plants, particularly in crops, less explored. In this study, we overexpressed AmCBF1 from Ammopiptanthus mongolicus (A. mongolicus) in wild type (R15), and found a significant darkening of leaf colour in transgenic plants (L28 and L30). RNA-seq analysis showed an enrichment of pathways associated with photosynthesis. Subsequent screening of differentially expressed genes revealed a significant up-regulation of GhClpR1, a gene linked to chloroplast development, in the transgenic strain. In addition, GhClpR1 was consistently expressed in upland cotton, with the highest expression observed in leaves. Subcellular localization analysis revealed that the protein encoded by GhClpR1 was located in chloroplasts. Yeast one hybrid and dual luciferase experiments showed that the AmCBF1 transcription factor positively regulates the expression of GhClpR1. VIGs-mediated silencing of GhClpR1 led to a significant yellowing phenotype in the leaves. This was accompanied by a reduction in chlorophyll content, and microscopic examination of chloroplast ultrastructure revealed severe developmental impairment. Finally, yeast two-hybrid assays showed that GhClpR1 interacts with the Clp protease complex accessory protein GhClpT2. Our study provides a foundation for studying the function of the Clp protease complex and a new strategy for cultivating high-light-efficiency cotton resources.

Genetic Landscape of the ACE2 Coronavirus Receptor.

BACKGROUND: SARS-CoV-2, the causal agent of COVID-19, enters human cells using the ACE2 (angiotensin-converting enzyme 2) protein as a receptor. ACE2 is thus key to the infection and treatment of the coronavirus. ACE2 is highly expressed in the heart and respiratory and gastrointestinal tracts, playing important regulatory roles in the cardiovascular and other biological systems. However, the genetic basis of the ACE2 protein levels is not well understood. METHODS: We have conducted the largest genome-wide association meta-analysis of plasma ACE2 levels in >28 000 individuals of the SCALLOP Consortium (Systematic and Combined Analysis of Olink Proteins). We summarize the cross-sectional epidemiological correlates of circulating ACE2. Using the summary statistics-based high-definition likelihood method, we estimate relevant genetic correlations with cardiometabolic phenotypes, COVID-19, and other human complex traits and diseases. We perform causal inference of soluble ACE2 on vascular disease outcomes and COVID-19 severity using mendelian randomization. We also perform in silico functional analysis by integrating with other types of omics data. RESULTS: We identified 10 loci, including 8 novel, capturing 30% of the heritability of the protein. We detected that plasma ACE2 was genetically correlated with vascular diseases, severe COVID-19, and a wide range of human complex diseases and medications. An X-chromosome cis-protein quantitative trait loci-based mendelian randomization analysis suggested a causal effect of elevated ACE2 levels on COVID-19 severity (odds ratio, 1.63 [95% CI, 1.10-2.42]; P=0.01), hospitalization (odds ratio, 1.52 [95% CI, 1.05-2.21]; P=0.03), and infection (odds ratio, 1.60 [95% CI, 1.08-2.37]; P=0.02). Tissue- and cell type-specific transcriptomic and epigenomic analysis revealed that the ACE2 regulatory variants were enriched for DNA methylation sites in blood immune cells. CONCLUSIONS: Human plasma ACE2 shares a genetic basis with cardiovascular disease, COVID-19, and other related diseases. The genetic architecture of the ACE2 protein is mapped, providing a useful resource for further biological and clinical studies on this coronavirus receptor.

Heat Shock Transcription Factor GhHSFB2a Is Crucial for Cotton Resistance to Verticillium dahliae.

Heat shock transcription factors (HSFs) play a critical regulatory role in many plant disease resistance pathways. However, the molecular mechanisms of cotton HSFs involved in resistance to the soil-borne fungus Verticillium dahliae are limited. In our previous study, we identified numerous differentially expressed genes (DEGs) in the transcriptome and metabolome of V. dahliae-inoculated Arabidopsis thaliana. In this study, we identified and functionally characterized GhHSFB2a, which is a DEG belonging to HSFs and related to cotton immunity to V. dahliae. Subsequently, the phylogenetic tree of the type two of the HSFB subfamily in different species was divided into two subgroups: A. thaliana and strawberry, which have the closest evolutionary relationship to cotton. We performed promoter cis-element analysis and showed that the defense-reaction-associated cis-acting element-FC-rich motif may be involved in the plant response to V. dahliae in cotton. The expression pattern analysis of GhHSFB2a displayed that it is transcriptional in roots, stems, and leaves and significantly higher at 12 h post-inoculation (hpi). Subcellular localization of GhHSFB2a was observed, and the results showed localization to the nucleus. Virus-induced gene silencing (VIGS) analysis exhibited that GhHSFB2a silencing increased the disease index and fungal biomass and attenuated resistance against V. dahliae. Transcriptome sequencing of wild-type and GhHSFB2a-silenced plants, followed by Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, protein-protein interaction, and validation of marker genes revealed that ABA, ethylene, linoleic acid, and phenylpropanoid pathways are involved in GhHSFB2a-mediated plant disease resistance. Ectopic overexpression of the GhHSFB2a gene in Arabidopsis showed a significant increase in the disease resistance. Cumulatively, our results suggest that GhHSFB2a is required for the cotton immune response against V. dahliae-mediated ABA, ethylene, linoleic acid, and phenylpropanoid pathways, indicating its potential role in the molecular design breeding of plants.

Repression of GhTUBB1 Reduces Plant Height in Gossypium hirsutum.

The original 'Green Revolution' genes are associated with gibberellin deficiency. However, in some species, mutations in these genes cause pleiotropic phenotypes, preventing their application in dwarf breeding. The development of novel genotypes with reduced plant height will resolve this problem. In a previous study, we obtained two dwarf lines, L28 and L30, by introducing the Ammopiptanthus mongolicus (Maxim. ex Kom.) Cheng f. C-repeat-binding factor 1 (AmCBF1) into the upland cotton variety R15. We found that Gossypium hirsutum Tubulin beta-1 (GhTUBB1) was downregulated in L28 and L30, which suggested that this gene may have contributed to the dwarf phenotype of L28 and L30. Here, we tested this hypothesis by silencing GhTUBB1 expression in R15 and found that decreased expression resulted in a dwarf phenotype. Interestingly, we found that repressing AmCBF1 expression in L28 and L30 partly recovered the expression of GhTUBB1. Thus, AmCBF1 expression presented a negative relationship with GhTUBB1 expression in L28 and L30. Moreover, yeast one-hybrid and dual-luciferase assays suggest that AmCBF1 negatively regulates GhTUBB1 expression by directly binding to C-repeat/dehydration-responsive (CRT/DRE) elements in the GhTUBB1 promoter, potentially explaining the dwarf phenotypes of L28 and L30. This study elucidates the regulation of GhTUBB1 expression by AmCBF1 and suggests that GhTUBB1 may be a new target gene for breeding dwarf and compact cultivars.

MicroRNA-1297 participates in the repair of intestinal barrier injury in patients with HIV/AIDS via negative regulation of PLCß1.

To explore the role of the miRNA-1297/phospholipase Cß1 (PLCß1) axis in intestinal barrier injury. Abnormally expressed miR-1297 and its target gene PLCß1 as well as their transcriptome sequencing were confirmed by bioinformatics analysis. Next, the intestinal barrier injury was induced by lipopolysaccharide (LPS) in the CCCHIE-2 cells. Subsequently, the impacts of miR-1297 and PLCß1 on the transcriptome were estimated. QRT-PCR and Western blotting were conducted to detect the relative mRNA and protein expressions, respectively. The cell viability and permeability were analyzed by MTT assay and fluorescent yellow detection. miR-1297 was significantly upregulated in patients with human immunodeficiency virus/acquired immunodeficiency syndrome and targeted PLCß1. Moreover, overexpressed PLCß1 was mainly enriched in the transforming growth factor-beta signaling pathway, while the knockdown of miR-1297 was focused on the arginine biosynthesis pathway. The overexpression of miR-1297 could reduce the PLCß1 expression and inhibit the viability of CCCHIE-2 cells injured by LPS, while the effect of the downregulation of miR-1297 was on the opposite. Western blotting and cell fluorescence localization experiments revealed that the inhibition of miR-1297 increased the expressions of PLCß1 and ZO-1. In addition, the upregulation of miR-1297 strengthened the permeability in cells injured by LPS, as did the knockdown of PLCß1. miR-1297 could restrain the repair of intestinal barrier injury via negatively regulating PLCß1 and its tight junction downstream protein ZO-1 in CCC-HIE-2 cells injured by LPS, which indicated that PLCß1 and miR-1297 might be important targets for the repair of intestinal barrier injury.

Connexin 43 participates in atrial electrical remodelling through colocalization with calcium channels in atrial myocytes.

Atrial fibrillation (AF) is associated with atrial conduction disturbances caused by electrical and/or structural remodelling. In the present study, we hypothesized that connexin might interact with the calcium channel through forming a protein complex and, then, participates in the pathogenesis of AF. Western blot and whole-cell patch clamp showed that protein levels of Cav1.2 and connexin 43 (Cx43) and basal ICa,L were decreased in AF subjects compared to sinus rhythm (SR) controls. In cultured atrium-derived myocytes (HL-1 cells), knocking-down of Cx43 or incubation with 30 mmol/L glycyrrhetinic acid significantly inhibited protein levels of Cav1.2 and Cav3.1 and the current density of ICa,L and ICa,T . Incubation with nifedipine or mibefradil decreased the protein level of Cx43 in HL-1 cells. Moreover, Cx43 was colocalized with Cav1.2 and Cav3.1 in atrial myocytes. Therefore, Cx43 might regulate the ICa,L and ICa,T through colocalization with calcium channel subunits in atrial myocytes, representing a potential pathogenic mechanism in AF.

Safety and efficacy of concomitant ablation for atrial fibrillation in rheumatic mitral valve surgery: A meta-analysis.

OBJECTIVES: This review aimed to evaluate the safety and efficacy of concomitant surgical ablation (SA) for patients with atrial fibrillation (AF) undergoing rheumatic mitral valve (MV) surgery. METHODS: A systematic search of relevant studies focusing on SA for patients with AF undergoing rheumatic MV surgery was performed. The primary outcomes included mortality, efficacy, and complications. RESULTS: Four randomized controlled trials (RCTs) and four observational studies covering 1931 patients met the inclusion criteria. In RCTs, no significant differences in reoperation for bleeding, low cardiac output syndrome, thromboembolic events, and early (risk ratio [RR], 2.07; 95% confidence intervals [CI], 0.37-11.40; p = .41) and midterm all-cause death (RR, 1.07; 95% CI, 0.40-2.88; p = .89) were noted between the SA group and the nonablation group. These results were similar to those obtained from observational studies. However, ablation was associated with a higher incidence of permanent pacemaker implantation (RR, 2.44; 95% CI, 1.15-5.18; p = .02) in observational studies but not in RCTs (RR, 2.03; 95% CI, 0.19-21.26; p = .56). Furthermore, additional SA was significantly more effective in sinus rhythm (SR) restoration than MV surgery alone at discharge and at the 12-month and 3-year follow-ups. CONCLUSIONS: Concomitant SA during rheumatic MV surgery does not increase perioperative adverse events. In addition, SA promotes considerable restoration of SR. Although some evidence exists that permanent pacemaker implantation is more common after ablation, not all studies support this notion.

Primeval outcomes of thoracoscopic transmitral myectomy with anterior mitral leaflet extension for hypertrophic obstructive cardiomyopathy.

BACKGROUND: The transaortic Morrow procedure is the current gold standard for hypertrophic obstructive cardiomyopathy (HOCM) patients who are resistant to maximum drug therapy. It is controversial whether concomitant mitral valve intervention is necessary. Only a few centers apply for concomitant anterior mitral leaflet extension with a bovine or autologous pericardial patch to further decrease systolic anterior motion. Our aim is to assess the primeval outcomes of thoracoscopic transmitral myectomy with anterior mitral leaflet extension (TTM-AMLE) in symptomatic HOCM patients. METHODS: Between April 2019 and November 2020, 18 consecutive HOCM patients who underwent TTM-AMLE were enrolled in this study. Preoperative, postoperative, and follow-up outcomes were compared and statistically analyzed. RESULTS: The mean age was (50.17 ± 6.18) years and 10 (55.56%) were males. 18 (100%) patients had mitral regurgitation preoperatively, and they all successfully underwent TTM-AMLE with a median cardiopulmonary bypass and aortic cross-clamp time of 200.0 (150.8, 232.0), and 127.5 (116.0, 149.0) min, respectively. The median length of ICU stay was 2.7 (1.4, 5.2) days. The interventricular septum thickness was significantly reduced (from 18.03 ± 3.02 mm to 11.91 ± 1.66 mm, p < .001). There was no perioperative mortality, perforation of ventricular septum, or conversion to sternotomy observed. During a median follow-up of 18 months (IQR, 5-24 months), 1 (5.56%) patient had severe mitral regurgitation due to patch detachment and received reoperation. Moderate degree of mitral regurgitation and more than 50 mmHg in left ventricular outflow tract gradient were found in 2 (11.11%), and 1 (5.56%) patients, respectively. 1 (5.56%) patient who had second-degree atrioventricular block received permanent pacemaker implantation postoperatively. Overall, the maximum left ventricular outflow tract gradient (88.50 [59.50, 112.75] mmHg vs. 10.50 [7.00, 15.50] mmHg, p = .002), left ventricular outflow tract velocity (4.70 [3.86, 5.33] m/s vs. 1.60 [1.33, 1.95] m/s, p < .001) and the degree of mitral regurgitation (6.99 ± 4.47 cm2 vs. 2.22 ± 1.51 cm2 , p = .001) were significantly decreased, with a significant reduction in the proportion of systolic anterior motion (94.44% vs. 16.67%, p < .001). CONCLUSIONS: The TTM-AMLE is a safe and effective surgical approach for selected patients with HOCM. In our series, it provides excellent relief of left ventricular outflow tract obstruction, while significantly eliminating mitral regurgitation. The early outcomes of TTM-AMLE are satisfactory, but further studies and longer follow-ups are awaited.

Activation of PKCα participates in the reduction of Ikur in atrial myocytes induced by tumour necrosis factor-α.

The atrial-specific ultra-rapid delayed rectifier K+ current (Ikur) plays an important role in the progression of atrial fibrillation (AF). Because inflammation is known to lead to the onset of AF, we aimed to investigate whether tumour necrosis factor-α (TNF-α) played a role in regulating Ikur and the potential signalling pathways involved. Whole-cell patch-clamp and biochemical assays were used to study the regulation and expression of Ikur in myocytes and in tissues from left atrial appendages (LAAs) obtained from patients with sinus rhythm (SR) or AF, as well as in rat cardiomyocytes (H9c2 cells) and mouse atrial myocytes (HL-1 cells). Ikur current density was markedly reduced in atrial myocytes from AF patients compared with SR controls. Reduction of Kv1.5 protein levels was accompanied by increased expression of TNF-α and protein kinase C (PKC)α activation in AF patients. Treatment with TNF-α dose-dependently reduced Ikur and protein expression of Kv1.5 but not Kv3.1b in H9c2 cells and HL-1 cells. TNF-α also increased activity of PKCα. Specific PKCα inhibitor Gö6976 alleviated the reduction in Ikur induced by TNF-α, but not the reduction in Kv1.5 protein. TNF-α was involved in the electrical remodelling associated with AF, probably by depressing Ikur in atrial myocytes via activation of PKCα.

Concomitant Transapical Transcatheter Aortic Valve Replacement and Transapical Balloon Mitral Valvuloplasty to Treat Severe Aortic Stenosis with Severe Mitral Stenosis.

This paper reports concomitant transapical transcatheter aortic valve replacement (TA-TAVR) and transapical balloon mitral valvuloplasty (TA-BMV) for the first time. A 72-year-old man with a diagnosis of rheumatic severe aortic stenosis with mild insufficiency and rheumatic severe mitral stenosis with mild insufficiency was referred to the Department of Cardiac Surgery of Guangdong Provincial People's Hospital. After the interdisciplinary discussion in the heart team (cardiac surgeon, cardiologist, anesthesiologist and image specialist), we decided to perform concomitant TAVR and BMV through one transapical approach considering the patient's preference, NYHA class IV heart failure, and the calculated perioperative risk (Euroscore II 3.74%, STS score for the combined mitral and aortic procedure is not available). No intraoperative or postoperative complications were observed.

Totally Thoracoscopic Redo Mitral Valve Replacement for a High-Risk Patient Following Failed MitraClip Procedure.

The wide adoption of the MitraClip procedure in clinical practice inevitably causes increases in surgical intervention demand for patients following failed MitraClip implantation. Current reports about surgical intervention after failed MitraClip procedure focused on open-heart surgery. In this case, totally thoracoscopic third-time redo mitral valve replacement was successfully performed for a high-risk patient, following aortic valve replacement and a failed MitraClip procedure.

High hydrostatic pressure induces atrial electrical remodeling through angiotensin upregulation mediating FAK/Src pathway activation.

Hypertension is an independent risk factor for atrial fibrillation (AF), although its specific mechanisms remain unclear. Previous research has been focused on cyclic stretch, ignoring the role of high hydrostatic pressure. The present study aimed to explore the effect of high hydrostatic pressure stimulation on electrical remodeling in atrial myocytes and its potential signaling pathways. Experiments were performed on left atrial appendages from patients with chronic AF or sinus rhythm, spontaneously hypertensive rats (SHRs) treated with or without valsartan (10 mg/kg/day) and HL-1 cells were exposed to high hydrostatic pressure using a self-developed device. Whole-cell patch-clamp recordings and western blots demonstrated that the amplitudes of ICa,L, Ito, and IKur were reduced in AF patients with corresponding changes in protein expression. Angiotensin protein levels increased and Ang1-7 decreased, while focal adhesion kinase (FAK) and Src kinase were enhanced in atrial tissue from AF patients and SHRs. After rapid atrial pacing, AF inducibility in SHR was significantly higher, accompanied by a decrease in ICa,L, upregulation of Ito and IKur, and a shortened action potential duration. Angiotensin upregulation and FAK/Src activation in SHR were inhibited by angiotensin type 1 receptor inhibitor valsartan, thus, preventing electrical remodeling and reducing AF susceptibility. These results were verified in HL-1 cells treated with high hydrostatic pressure, and demonstrated that electrical remodeling regulated by the FAK-Src pathway could be modulated by valsartan. The present study indicated that high hydrostatic pressure stimulation increases AF susceptibility by activating the renin-angiotensin system and FAK-Src pathway in atrial myocytes.

VdOGDH is involved in energy metabolism and required for virulence of Verticillium dahliae.

Verticillium dahliae, a soil-borne fungus, can invade plant vascular tissue and cause Verticillium wilt. The enzyme α-oxoglutarate dehydrogenase (OGDH), catalyzing the oxidation of α-oxoglutarate in the tricarboxylic acid cycle (TCA), is vital for energy metabolism in the fungi. Here, we identified the OGDH gene in V. dahliae (VdOGDH, VDAG_10018) and investigated its function in virulence by generating gene deletion mutants (ΔVdOGDH) and complementary mutants (ΔVdOGDH-C). When the ΔVdOGDH mutants were supplemented with different carbon sources, vegetative growth on Czapek Dox medium was significantly impaired, suggesting that VdOGDH is crucial for vegetative growth and carbon utilization. Conidia of the ΔVdOGDH mutants were atypically rounded or spherical, and hyphae were irregularly branched and lacked typical whorled branches. Mutants ΔVdOGDH-1 and ΔVdOGDH-2 were highly sensitive to H2O2 in the medium plates and had higher intracellular ROS levels. ΔVdOGDH mutants also had elevated expression of oxidative response-related genes, indicating that VdOGDH is involved in response to oxidative stress. In addition, the disruption of VdOGDH caused a significant increase in the expression of energy metabolism-related genes VdICL, VdICDH, VdMDH, and VdPDH and melanin-related genes Vayg1, VdSCD, VdLAC, VT4HR, and VaflM in the ΔVdOGDH mutants; thus, VdOGDH is also important for energy metabolism and melanin accumulation. Cotton plants inoculated with ΔVdOGDH mutants exhibited mild leaf chlorosis and the disease index was lower compared with wild type and ΔVdOGDH-C strains. These results together show that VdOGDH involved in energy metabolism of V. dahliae, is also essential for full virulence by regulating multiple fungal developmental factors.

Modified unicaval drainage in reoperative isolated tricuspid valve repair via totally thoracoscopic approach.

AIM: The aim of this study was to investigate the feasibility, safety, and clinical effect of modified unicaval drainage for thoracoscopic reoperative isolated tricuspid valve repair, compared with conventional bicaval drainage. METHODS: A total of 45 consecutive cases of patients who underwent thoracoscopic reoperative isolated tricuspid valve repair on beating-heart were enrolled and divided into two groups according to the different venous drainage (Group A: modified unicaval drainage, Group B: conventional bicaval drainage). A retrospective analysis of perioperative data and clinical outcomes were performed and all the surviving cases were followed up. Re-evaluation of echocardiography and electrocardiogram was performed prior to discharge, and at first month, sixth month, and every year follow-up. RESULTS: The overall postoperative 30-day mortality was 4.5% in Group A and 8.7% in Group B. The postoperative tricuspid valve regurgitation grade of both groups decreased significantly from preoperative regurgitation grade, p < 0.001, without intergroup significant difference, p = 0.815. Follow-up duration ranged from 6 to 38 months, there was one death at 24 months in Group A, and another at 9 months in Group B, respectively. Nobody from both groups experienced reintervention for residual tricuspid regurgitation. No significant difference could be identified about the incidence of postoperative morbidities and follow-up adverse events. CONCLUSION: Both strategies of caval venous drainage can provide satisfactory exposure for thoracoscopic reoperative isolated tricuspid valve repair and equivalent favorable postoperative outcome. And the modified unicaval drainage group may even preserve the anesthetic time and decrease the risk of iatrogenic jugular injury, achieving a more simplified procedure with better cosmetic outcome.

Outcomes of Totally Endoscopic Beating-Heart Tricuspid Repair in Redo Cardiac Surgery.

BACKGROUND: The role of endoscopic surgery in treating late severe tricuspid regurgitation after cardiac surgery has not been well investigated. The aim of this study was to evaluate the outcomes of a combination of a beating-heart, minimally invasive approach and a leaflet-augmentation technique in treating tricuspid regurgitation after cardiac surgery. METHOD: This was a retrospective cohort study. From January 2015 to July 2018, patients undergoing reoperative tricuspid valve repair with a totally endoscopic approach were enrolled. Procedures were performed on beating hearts with normothermic cardiopulmonary bypass (CPB). RESULTS: A total of 43 adults (mean age 53.4±11.4 yr; 9 men) met the inclusion criteria. The interval between prior cardiac surgery and current tricuspid repair was 17.6±6.5 years. Ten (10) patients had previous tricuspid repair and concomitant previous cardiac surgery. In the current endoscopic approach, tricuspid repair techniques included 38 leaflet augmentations, 38 annular ring placements, five artificial chordae, one cleft closure, five commissure recreations, and eight papillary muscle relaxations. Mean CPB time, median ventilation time, and median hospital stay were 128.5±54.2 minutes, 20.5 hours (range, 6-436 hrs), and 7 days (range, 4-56 d), respectively. There were only three in-hospital deaths and no follow-up mortality. The regurgitant jet area was decreased from 21.5±12.1 cm2 preoperatively to 2.4±2.2 cm2 postoperatively (p<0.001). In patients with previous tricuspid repair, although the technique of valvuloplasty seems more complex, CPB time, procedure time and hospital stay were not longer than in patients who did not have previous tricuspid repair. CONCLUSIONS: Beating-heart, video-assisted, minimal access tricuspid repair after previous cardiac surgery is feasible, reproducible, and associated with low mortality, even in patients who have had previous tricuspid repair.

Novel role of the clustered miR-23b-3p and miR-27b-3p in enhanced expression of fibrosis-associated genes by targeting TGFBR3 in atrial fibroblasts.

Atrial fibrillation (AF) is the most common type of arrhythmia in cardiovascular diseases. Atrial fibrosis is an important pathophysiological contributor to AF. This study aimed to investigate the role of the clustered miR-23b-3p and miR-27b-3p in atrial fibrosis. Human atrial fibroblasts (HAFs) were isolated from atrial appendage tissue of patients with sinus rhythm. A cell model of atrial fibrosis was achieved in Ang-II-induced HAFs. Cell proliferation and migration were detected. We found that miR-23b-3p and miR-27b-3p were markedly increased in atrial appendage tissues of AF patients and in Ang-II-treated HAFs. Overexpression of miR-23b-3p and miR-27b-3p enhanced the expression of collagen, type I, alpha 1 (COL1A1), COL3A1 and ACTA2 in HAFs without significant effects on their proliferation and migration. Luciferase assay showed that miR-23b-3p and miR-27b-3p targeted two different sites in 3'-UTR of transforming growth factor (TGF)-ß1 receptor 3 (TGFBR3) respectively. Consistently, TGFBR3 siRNA could increase fibrosis-related genes expression, along with the Smad1 inactivation and Smad3 activation in HAFs. Additionally, overexpression of TGFBR3 could alleviate the increase of COL1A1, COL3A1 and ACTA2 in HAFs after transfection with miR-23b-3p and miR-27b-3p respectively. Moreover, Smad3 was activated in HAFs in response to Ang-II treatment and inactivation of Smad3 attenuated up-regulation of miR-23b-3p and miR-27b-3p in Ang-II-treated HAFs. Taken together, these results suggest that the clustered miR-23b-3p and miR-27b-3p consistently promote atrial fibrosis by targeting TGFBR3 to activate Smad3 signalling in HAFs, suggesting that miR-23b-3p and miR-27b-3p are potential therapeutic targets for atrial fibrosis.

Invasive therapies for patients with concomitant heart failure and atrial fibrillation.

Atrial fibrillation (AF) and heart failure (HF) are two clinical entities that can present either separately or concurrently. One entity can lead to the other and vice versa as AF can not only be the underlying etiology of HF but also exacerbate HF due to other cardiac diseases. Besides prevention of cerebral and systemic embolism and elimination of AF-related symptoms, restoration of sinus rhythm for AF patients helps to avoid or reduce HF, irrespective of their underlying heart disease. Successful rates of medical therapy for AF are low in persistent AF, and much lower in long-standing AF, while invasive procedures for AF yield promising results. In this review, the authors evaluate the value of invasive therapies for HF patients complicated with non-valvular AF. We examine this clinical problem by interpreting the relationships between these two entities: the mechanism of tachycardia-induced cardiomyopathy (TIC), past opinions about rhythm control and rate control of AF, discrimination of HF-related AF and AF-induced HF, how to identify the AF patients that could benefit from invasive therapies, and how to select invasive therapies for different AF patients and peri-operative treatments.

Intraoperative Implantation of Temporary Endocardial Pacing Catheter During Thoracoscopic Redo Tricuspid Surgery.

BACKGROUND: The placement of a temporary epicardial pacing wire is a challenge during a minimally invasive redo cardiac operation. The aim of this study is to assess the application of temporary endocardial pacing in patients who underwent minimally invasive redo tricuspid surgery. METHODS: Perioperative data of consecutive patients who underwent thoracoscopic redo tricuspid surgery were collected. All the tricuspid surgeries and combined procedures were performed under peripheral cardiopulmonary bypass without aortic cross-clamping. A sheath was introduced into the right jugular vein beside the percutaneous superior vena cava cannula and a temporary endocardial pacing catheter was guided into the right ventricle via the sheath prior to the right atrial closure. The pacemaker was connected and run as needed during or after operation. RESULTS: A total of 33 patients who underwent thoracoscopic redo tricuspid surgery were enrolled. Symptomatic tricuspid valve regurgitation (93.9%) and tricuspid valvular prosthesis obstruction (6.1%) after previous cardiac operations were noted as indications for a redo surgery. The mean time from previous cardiac operation to this time redo surgery was 13.3±6.4years. Isolated tricuspid valve replacement was performed in 18 patients (54.5%) and tricuspid valve plasty combined with or without mitral valve replacement was performed in 15 patients (45.5%). A temporary endocardial pacing catheter was successfully placed in the right ventricle for all patients with good sensing and pacing. No temporary pacing related complications occurred from insertion to removal of pacing catheter in the patients. CONCLUSIONS: This application of temporary endocardial pacing provided a safe and effective substitute for epicardial pacing in patients who underwent minimally invasive redo tricuspid surgery.