Background Valvular heart disease, particularly aortic valve disease including stenosis and regurgitation, is a common heart disease. This study aimed to explore the protein profiling and the biomarkers in severe aortic valve disease and to provide new insights into the therapeutic strategy. Methods Blood samples from 80 subjects were collected and analyzed by data independent acquisition technique in 3 comparisons (mild/moderate‐control, severe‐control, and severe–mild/moderate) and validated by ELISA. The diagnostic value of differentially expressed proteins associated with severe valvular heart disease was also evaluated by the receiver operating characteristic curve. Results A total of 9976 peptides and 451 proteins were identified through liquid chromatography‐tandem mass spectrometry analysis. From these, 64 in mild/moderate‐control, 50 in severe‐control, and 50 in severe–mild/moderate comparisons were identified as differentially expressed proteins. IGFBP7 (insulin‐like growth factor‐binding protein 7; 5581.0±697.0 ng/mL), DSG1 (desmoglein‐1; 21.0±2.0 pg/mL), ADIPOQ (adiponectin; 26 686.0±3730 ng/mL), and JUP (junction plakoglobin; 10.2±0.6 ng/mL) levels in the severe group were significantly higher than that in the mild/moderate (P<0.05) group. Additionally, ADIPOQ and JUP levels in the severe group were also higher than that in control (P<0.001). Receiver operating characteristic curve analysis showed that IGFBP7, DSG1, JUP, and ADIPOQ had strong potential value to be associated with severe aortic valve disease. Conclusions By constructing proteomics profile to identify the protein characteristics this study found that increased IGFBP7, DSG1, JUP, and ADIPOQ are the characteristics of proteins in patients with severe valvular heart disease. These findings provide new insight into the diagnosis and pathogenesis of valvular heart disease, particularly aortic valve disease.

BACKGROUND:For patients undergoing surgical valve procedures with concomitant coronary artery disease, current guidelines recommend that coronary artery bypass grafting (CABG) should be anatomically guided on the basis of stenosis severity, as assessed by coronary angiography. We aimed to test whether a physiologically guided strategy using angiography-derived fractional flow reserve (FFR) could improve clinical outcomes in this population. METHODS:FAVOR IV-QVAS is an investigator-initiated, multicentre, randomised, triple-blind trial done at 12 tertiary hospitals in China. Eligible patients were aged 18 years or older and were scheduled for valve surgery, with at least one clinically significant stenosis in a major coronary artery. Patients were randomly assigned (1:1) to undergo physiologically guided CABG (for lesions with an angiography-derived FFR value ≤0·80) or anatomically guided CABG (for lesions with a stenosis diameter ≥50% on coronary angiography). Randomisation was done using a web-based program and stratified by site with fixed blocks of four. Patients, surgeons, follow-up physicians, and outcome assessors were masked to treatment allocation. The primary outcome was a composite of death, myocardial infarction, stroke, unplanned coronary revascularisation, and new renal failure requiring dialysis within 30 days after surgery. The key secondary outcome was a composite of death, myocardial infarction, stroke, unplanned coronary revascularisation, and hospitalisation for unstable angina or heart failure at a minimum follow-up of 1 year. The primary analysis of the primary and key secondary outcomes was done in a modified intention-to-treat population that included all randomly assigned patients who underwent surgery and had available data for the primary outcome. Missing data for the primary outcome were planned to be analysed using complete-case analysis or multiple imputation, with a proportion of missing data of 2% as the threshold. This trial is registered at ClinicalTrials.gov (NCT03977129); extended follow-up is ongoing. FINDINGS:Between Aug 4, 2019, and Aug 13, 2024, 793 patients were enrolled. 396 were randomly assigned to the angiography-derived FFR group and 397 to the coronary angiography group; one patient in the coronary angiography group declined surgery and was excluded from the modified intention-to-treat population. The median age was 65 years (IQR 59-70), 221 (28%) patients were female, and 571 (72%) were male. Concomitant CABG was done in 223 (56%) patients in the angiography-derived FFR group and in 388 (98%) patients in the coronary angiography group. The primary outcome occurred in 31 (7·8%) patients in the angiography-derived FFR group and 53 (13·4%) in the coronary angiography group (absolute difference -5·6 percentage points [95% CI -9·9 to -1·3]; risk ratio 0·58 [95% CI 0·38 to 0·89]; p=0·011). Death within 30 days occurred in 11 (2·8%) patients in the angiography-derived FFR group and 17 (4·3%) patients in the coronary angiography group. At a median follow-up of 27 months (28 months [IQR 18-44] in the angiography-derived FFR group and 27 months [18-42] in the coronary angiography group), the key secondary outcome occurred in 82 (20·7%) patients in the angiography-derived FFR group and in 106 (26·8%) patients in the coronary angiography group (hazard ratio 0·74 [95% CI 0·55-0·98]; p=0·036). INTERPRETATION:Among patients undergoing valve surgery with concomitant coronary artery disease, physiologically guided CABG using angiography-derived FFR reduced the incidence of the composite perioperative outcome compared with anatomically guided CABG. These findings support a selective approach to surgical coronary revascularisation guided by physiological assessment in patients undergoing valve procedures. FUNDING:Shanghai Hospital Development Center, Shanghai Municipal Science and Technology Commission, and Ministry of Science and Technology of the People's Republic of China.

BACKGROUND:Septal myectomy is the gold standard treatment for drug-refractory obstructive hypertrophic cardiomyopathy (oHCM). However, conventional septal myectomy (CSM) has been largely confined to specialized centers owing to its technical complexity. Transapical beating-heart septal myectomy (TA-BSM) can simplify CSM, enabling minimally invasive tailored septal resections in the beating heart under real-time echocardiographic guidance. Despite single-institution experience showed favorable efficacy and safety, whether TA-BSM can achieve similar clinical outcomes as CSM remains unknown since randomized controlled trial comparing the 2 approaches was unavailable. METHODS:The TAILOR-HCM trial (Transapical Beating-Heart Septal Myectomy vs Conventional Surgical Myectomy in Patients with Obstructive Hypertrophic Cardiomyopathy) is a multicenter, randomized, controlled, assessor-blinded, noninferiority trial evaluating the safety and efficacy of a novel device-based TA-BSM procedure conducted at 11 experienced CSM centers in China. In total, 216 symptomatic patients with oHCM who meet guideline-directed indications for septal myectomy will be randomly assigned in a 1:1 ratio to TA-BSM or CSM. The primary endpoint is relief of left ventricular outflow tract (LVOT) obstruction at 12 months, defined as a resting LVOT gradient <30 mm Hg and a standardized Valsalva maneuver-provoked LVOT gradient <50 mm Hg. Secondary endpoints include cardiac hemodynamic and structural parameters, procedure-related outcomes, quality of life, and laboratory examinations. The key safety outcome is all-cause mortality within 12 months after surgery. CONCLUSIONS:TAILOR-HCM is the first multicenter randomized controlled trial evaluating both TA-BSM and CSM in oHCM. Through comparative evidence against CSM, this study will inform future clinical decision-making. If noninferior hemodynamic efficacy with favorable safety is confirmed, TA-BSM may represent an alternative surgical approach that expands therapeutic options and improves access to definitive septal reduction therapy for patients with oHCM. CLINICAL TRIAL REGISTRATION:https://www.chictr.org.cn. Unique Identifier: ChiCTR2400087414.

OBJECTIVES:We evaluated the safety and efficacy of transcatheter aortic valve replacement (TAVR) up to 1-year follow-up for patients with severe pure aortic valve regurgitation (AR) or mixed severe aortic valve regurgitation and aortic valve stenosis (AR+AS) using a novel self-expandable bioprosthesis. METHODS:From 2021 to 2022, transapical TAVR using Ken-Valve (Jenscare Biotechnology Ltd, Ningbo, China) was performed in 142 symptomatic patients (mean age 70.3 ± 5.5 years) with pure AR (n = 109) or AR+AS (n = 33) across 15 hospitals in China. All patients were considered high-risk or inoperable after heart team evaluation, with a mean Society of Thoracic Surgeons score of 5.9 ± 3.0%, and 99.3% in NYHA class III/IV. Procedural characteristics, echocardiography data, and clinical outcomes up to 1-year were analysed. RESULTS:Technical success was achieved in 97.2% of cases. Two (1.4%) patients were converted to open surgery due to unsuitable anatomy or valve migration during the procedure. New permanent pacemakers were implanted in 20 (14.1%) patients. Three (2.1%) patients had stroke, and 3 (2.1%) patients had major bleeding. Thirty-day mortality was 2.1%, and all-cause mortality at 1-year was 5.6% (8/142). Mean aortic valve gradient and effective orifice area (EOA) at 1-year postoperatively were 9.4 ± 5.4 mmHg and 1.9 ± 0.6 cm2, respectively. Significant improvement in clinical symptoms, positive left ventricular remodelling, and quality of life were observed up to 1-year. There was no significant difference in mortality, complications, and haemodynamic performance between patients with pure AR and AR+AS at 1-year. CONCLUSIONS:TAVR using the Ken-Valve was safe and effective in patients with pure AR or mixed AR+AS in mid-term. CLINICAL REGISTRATION NUMBER:NCT03788590.

Infective endocarditis (IE) remains a life-threatening condition, particularly in complex cases with destruction of the aorto-mitral curtain (AMC), also known as the intervalvular fibrous body (IVFB). Multiple factors have contributed to an increased incidence of IE and more extensive destruction of the valvular apparatus, necessitating more aggressive surgical intervention. Thus, this study aimed to evaluate the role and outcomes of the Commando procedure in managing IE involving the AMC. A narrative literature review was conducted to provide a comprehensive overview of the Commando procedure in IE involving the AMC, focusing on recent trends, indications, operative strategies, and outcomes. The keywords "infective endocarditis", "Commando procedure", "aorto-mitral curtain", "intervalvular fibrous body", and "double-valve replacement" were searched in PubMed, Web of Science, and Google Scholar. Only English language studies were included. Inclusion criteria comprised studies involving IE patients who underwent the Commando procedure or any associated modified version; studies reporting conventional double-valve replacement (DVR) performed for IE without AMC involvement were also included for comparison. Exclusion criteria included patients who underwent the Commando procedure for non-infection indications, such as small annuli or calcification. Commando surgery was associated with a 30-day mortality of 9-32%, with 1-, 5-, and 10-year survival rates of 55.4-92.9%, 37.7-68%, and 37-48%, respectively. High-risk factors included infection by specific microorganisms and the need for emergency surgery. The Hemi-Commando procedure demonstrated lower early mortality (8-13.6%), higher 1-year survival (77.5-91%), and 92.3% freedom from reoperation at 1-3 years. Compared with DVR, the Commando procedure had higher operative mortality but similar long-term survival after risk adjustment. Despite the associated high perioperative risks, the Commando surgical procedure remains critical for managing complex IE with AMC destruction. Modified techniques may balance infection control and functional preservation, potentially improving survival in selected patients. Future research should focus on standardized surgical protocols, long-term durability, and multidisciplinary collaboration to optimize outcomes.

BACKGROUND:Fibrosis is one of the major causes of cardiac allograft malfunction and is mainly driven by fibroblasts. However, the role of recipient-derived cells in generating allograft fibroblasts and the underlying mechanisms remain to be explored. METHODS:We analyzed human heart allograft samples and used murine transplant models (C57BL/6J, Cd34 (cluster of differentiation 34)-CreERT2; R26-tdTomato, mRFP (cell membrane labeled with red fluorescence protein) mice, Rosa26-iDTR, Postn-CreERT2; R26-tdTomato, double-tdTomato, and immunodeficient mice with BALB/c donors). Human progenitor cells were cultivated from blood. Single-cell RNA sequencing, Western blotting, quantitative polymerase chain reaction, and immunohistochemistry, whole-mount staining with 3-dimensional reconstruction, and in vivo/in vitro experiments were applied to characterize allograft cellular composition and communication. RESULTS:Single-cell RNA sequencing was introduced to delineate the allograft cell atlas of patients and mice. Y chromosome analysis identified that recipient-derived cells contributed to allograft fibroblasts in both patients and murine models. Combining the genetic cell lineage tracing technique, we found that recipient-derived CD34+ cells could give rise to activated fibroblasts. Bone marrow transplantation and parabiosis models revealed that the recipient's circulating non-bone marrow Cd34+ cells could generate allograft fibroblasts. Human CD34+ cells could differentiate into fibroblasts both in vivo and in vitro. CD34+ fibroblast progenitors were recruited by CXCL12 (C-X-C motif chemokine ligand 12)-ACKR3 (atypical chemokine receptor 3) and MIF (macrophage migration inhibitory factor)-ACKR3 interactions and differentiated via the TGFβ (transforming growth factor beta)/GFPT2 (glutamine-fructose-6-phosphate transaminase 2)/SMAD2/4 (small mother against decapentaplegic 2/4) axis. Ablation of recipient Cd34+ cells reduced activated fibroblasts and alleviated allograft fibrosis. CONCLUSIONS:We identify circulating CD34+ cells as a novel source of fibroblast progenitors that contribute to cardiac allograft fibrosis, suggesting that targeting recipient CD34+ cells could be a novel therapeutic potential for treating cardiac fibrosis after heart transplantation.

Atrial fibrillation (AF) significantly increases stroke risk, particularly through left atrial appendage (LAA) involvement. This trial evaluated the safety and efficacy of the Perclip system for LAA exclusion in Chinese AF patients. This prospective study recruited patients with AF and CHA2DS2-VASc scores ≥ 2 who required conventional concomitant open-heart surgery or AF surgery through thoracoscopy at nine centers in China. The Perclip LAA occlusion system was implanted during surgery and follow-ups were scheduled at 30 days and 3, 6, and 12 months after surgery. The primary efficacy endpoint was the complete LAA closure rate at 3 months after surgery. The primary safety endpoint was the incidence of device-related serious adverse events within 30 days after surgery. Perclip implantation was performed on 76 participants (concomitantly with open-heart surgery in 65 participants). The device was successfully implanted in all subjects. The complete LAA closure rate was 98.7

Atrial fibrillation (AF) is the most common sustained arrhythmia, conferring risks of stroke and heart failure. Monocyte activation-associated inflammation is implicated in AF, yet the recruitment of monocytes and their role in atrial remodeling remain unclear. Here we show that monocytes from AF patients upregulate phospholipase C gamma 2 (PLCG2). In a combined AF male mouse model, phospho-PLCγ2+ monocytes are recruited to the atria, where they trigger endothelial‑to‑mesenchymal transition (EndMT) through the secreted phosphoprotein 1 (SPP1)-integrin α9β1 signaling axis. Monocyte-specific deletion of PLCG2 blocks atrial recruitment of these monocytes and reduces AF. Depletion of the gut microbiota with antibiotics reduces the number of phospho-PLCγ2+ monocytes in the atria, suppresses EndMT, and attenuates AF inducibility, and these effects are reversed by fecal microbiota transplantation (FMT). Mechanistically, gut microbiota-derived bacterial membrane vesicles activate spleen tyrosine kinase (Syk)/PLCG2 signaling in monocytes. These findings establish a gut microbiota-monocyte-EndMT axis, wherein monocyte-endocardial crosstalk drives AF. Atrial fibrillation involves systemic inflammatory activation that remodel the atrial endocardium. Here, the authors show that gut microbiota activate PLCy2 positive monocytes, promoting endothelial-to-mesenchymal transition and atrial fibrillation through a microbiota–monocyte–endocardial axis.

Background For patients with severe degenerative mitral regurgitation (DMR) at prohibitive or high surgical risk, transcatheter edge-to-edge repair (TEER) has become an effective alternative. The GeminiOne is a novel TEER device featuring a unique groove-cam mechanism. Objectives This study reports the primary, secondary, and 1-year outcomes of the GeminiOne-DMR (Safety and Efficacy of the GeminiOne Transcatheter Valve Edge-to-Edge Repair System in Patients With Moderate-severe or Severe Degenerative Mitral Regurgitation) trial. Methods A total of 120 patients with prohibitive surgical risk and DMR grade ≥3+ were enrolled and evaluated by an independent echocardiography core laboratory and a clinical event committee. The primary endpoint was clinical success, defined as freedom from all-cause mortality, mitral valve reintervention, and mitral regurgitation >2+ at 1-year follow-up. Results At 1 year, the clinical success rate was 89.84% ± 2.78% (95% CI: 84.56%-95.46%), meeting the prespecified primary efficacy endpoint. The rates of freedom from 1-year all-cause mortality, major adverse events, mitral valve reintervention, and heart failure hospitalization were 97.48% ± 1.35%, 91.61% ± 2.54%, 98.31% ± 1.02%, and 94.00% ± 2.20%, respectively. Mitral regurgitation ≤2+ was achieved in 92.24% of patients at 1 year. Significant improvements were observed in functional and quality-of-life outcomes, with the proportion of patients classified as NYHA funcional class I/II increasing from 23.33% at baseline to 94.74% at 1 year (P < 0.001), and Kansas City Cardiomyopathy Questionnaire scores also improving significantly from baseline to 1 year (P < 0.001). Conclusions This trial demonstrated the initial safety and efficacy of the GeminiOne TEER system for treating significant symptomatic DMR in patients at prohibitive or high surgical risk. (Safety and Efficacy of the GeminiOne Transcatheter Valve Edge-to-Edge Repair System in Patients With Moderate-severe or Severe Degenerative Mitral Regurgitation; NCT05655897)

This study evaluated the safety and efficacy of the Renatus transcatheter aortic valve system in treating severe aortic stenosis. This prospective, multicenter, single-arm clinical trial employed a target-value approach. The primary endpoint was the all-cause mortality rate at one year postoperatively, while secondary endpoints included assessments of safety and effectiveness. Safety was measured by the all-cause mortality rate at 30 days, the incidence of major adverse cardiovascular events within one year, and the device success rate. Effectiveness was assessed using transvalvular pressure gradient measurements, the incidence of paravalvular leaks, improvements in New York Heart Association (NYHA) cardiac function classification, and quality of life assessments. The study enrolled 166 patients across 14 national centers between July 2021 and April 2022, with a mean age of 73.9 ± 6.0 years and a median STS risk score of 7.7

RNA m6A modification plays a vital role in regulating cardiac function; however, its comprehensive mechanisms require further exploration. We observed that the expression of METTL3, a m6A methyltransferase, is significantly increased in hypertrophic hearts as well as during phenylephrine (PE)-induced cardiomyocyte hypertrophy in neonatal rat ventricular myocytes and transverse aortic constriction (TAC)-induced cardiac hypertrophy in mice. Concordantly, METTL3 knockdown could significantly inhibit PE-induced cardiomyocyte hypertrophy. RNA m6A-RIP-Seq analysis revealed that METTL3 may regulate lipid metabolism in cardiomyocytes by methylating the mRNA of fatty acid synthase (FASN) and stearoyl-CoA desaturase 1 (SCD1), thereby enhancing their stability. We developed a platelet liposome fusion membrane carrier that is loaded with siMETTL3. This carrier significantly reduces the expression of FASN and SCD1, enhances fatty acid oxidation, and promotes ATP production in cardiomyocytes. Overexpression of FASN and SCD1 can partially alleviate the impact on the aforementioned fatty acid oxidation-related effects caused by siMETTL3 platelet liposome fusion membrane carrier. Consequently, our siMETTL3 carrier alleviates TAC-induced pathological hypertrophy and improves cardiac function in vivo. These findings advance our understanding of METTL3-mediated RNA m6A modification in cardiac hypertrophy, holding promise for future treatments through our gene delivery carrier related to pathological cardiac hypertrophy.

Quadricuspid aortic valve (QAV) is rare. However, to repair a quadricuspid aortic valve is not as easy to realize as in bicuspid aortic valve. The surgical design is crucial to rebuild the stable structure. Here we present a case of repair of quadricuspid aortic valve using the strategy of tricuspidization.

BACKGROUND:Cardiac hypertrophy is accompanied by profound metabolic remodeling, including enhanced glycolysis. Histone lactylation, a posttranslational modification linked to glycolytic activity, has been shown to regulate gene transcription. However, its role in cardiac hypertrophy remains unclear. METHODS:Histone lactylation was assessed in failing human and mouse hearts. Male mice subjected to transverse aortic constriction were treated with oxamate (an LDHA [lactate dehydrogenase A] inhibitor) or sodium lactate to modulate histone lactylation. Cardiomyocyte-specific Ldha deletion was also evaluated. In vitro, phenylephrine-stimulated neonatal rat ventricular myocytes were used to examine the effects of lactylation inhibition. Potential histone lactylation transferases were identified by coimmunoprecipitation. Promoter-specific histone lactylation was analyzed by Cleavage Under Targets and Tagmentation and ChIP quantitative polymerase chain reaction, and transcriptional regulation was further evaluated by nascent RNA-seq. TGFB2 (transforming growth factor β2) function was investigated using AAV-shRNA knockdown and lentiviral overexpression in combination with pharmacological inhibition of PI3K (phosphoinositide 3-kinase) or AKT (protein kinase B). RESULTS:Histone lactylation was elevated in failing human and mouse hearts. Reducing lactylation attenuated transverse aortic constriction-induced hypertrophy and fibrosis, preserving cardiac function, whereas increasing lactylation exacerbated pathological remodeling. In vitro, inhibition of lactylation suppressed phenylephrine-induced cardiomyocyte hypertrophy. P300 and GCN5 (general control non-derepressible 5) were identified as candidate lactylation transferases. Cleavage Under Targets and Tagmentation revealed lactate-dependent enrichment of H3K18la (histone H3 lysine 18 lactylation) at the TGFB2 promoter, correlating with increased TGFB2 expression. Cardiac-specific Tgfb2 knockdown reversed the prohypertrophic effects of histone lactylation in vivo, while Tgfb2 overexpression promoted cardiomyocyte hypertrophy via PI3K/AKT/mTOR (mechanistic target of rapamycin) signaling. Pharmacological inhibition of PI3K or AKT attenuated this effect. CONCLUSIONS:Histone lactylation promotes pathological cardiac hypertrophy and heart failure by upregulating TGFB2 and activating PI3K/AKT/mTOR signaling. These findings identify histone lactylation as an epigenetic link between metabolic reprogramming and hypertrophic signaling, and suggest it as a potential therapeutic target for pathological cardiac remodeling.

PURPOSE:We aimed to identify the preoperative risk factors for hypoxemia during one-lung ventilation (OLV) in patients who underwent thoracoscopic radical resection for lung cancer and to establish a prediction model. METHODS:This retrospective study included 268 patients who underwent video-assisted thoracoscopic surgery (VATS) radical resection for lung cancer at Yunnan Cancer Hospital from October 2021 to June 2022. Logistic regression analysis was performed to identify independent preoperative risk factors for hypoxemia during OLV. A prediction model was established, and its predictive efficacy was evaluated with the consistency index (C-index) and the area under the receiver operating characteristic curve (AUC). RESULTS:The multivariate analysis demonstrated that the ratio of dependent lung FLV to total lung FLV (odds ratio [OR] 0.8434; 95% confidence interval [CI] 0.7281-0.9623), dependent lung HU value (OR 0.9676; 95% CI 0.9419-0.9895), dependent lung LAV% (OR 1.1838; 95% CI 1.0856-1.3138), and DLCO% pred (OR 0.9632; 95% CI 0.9353-0.9864) were independent preoperative risk factors affecting OLV hypoxemia. The prediction model that was constructed by this indicator was internally validated, with a C-index of 0.963, an AUC of 0.96 (95% CI 0.94-0.99) for the training set, and an AUC of 0.92 (95% CI 0.83-1) for the test set. CONCLUSION:CT-based quantitative indicators of the dependent lung are strong predictors of hypoxemia during OLV for lung cancer patients. This prediction model helps anesthesiologists to intuitively and accurately identify patients who may experience hypoxemia during OLV before surgery and develop individualized management strategies.

Introduction: With the accruing experience of the single femoral venous drainage (SFVD) technique in reoperative isolated tricuspid valve surgery via a minimally invasive approach, some surgeons applied it to patients undergoing primary surgery. The aim of our study was to evaluate the hematological and clinical effects of SFVD in minimally invasive mitral valve surgery combined with tricuspid annuloplasty.Methods: A total of 99 consecutive patients undergoing minimally invasive mitral valve surgery requiring concomitant tricuspid annuloplasty at our institution between January 2016 and December 2020 were retrospectively analyzed. The patients were divided into two groups according to the different venous drainage strategies: Group S (n = 53), in which venous drainage via single femoral venous cannulation, and Group D (n = 46), in which venous drainage via superior vena cava combined with femoral venous cannulations with caval snaring. The postoperative hematological parameters and postoperative complications were compared between the two groups. Multivariate stepwise linear regression was performed to determine whether SFVD independently predicted postoperative hemoglobin drop and operation time.Results: The red blood cell counts, hemoglobin, and hematocrit levels were significantly lower in Group S on arrival at the intensive care unit (ICU) (p = 0.048; p = 0.009; p = 0.016, respectively), while no significant difference between the two groups on the first postoperative day. Multivariate linear regression indicated that the use of SFVD was independently positively associated with hemoglobin drop (B = 6.15, 95% CI: 2.47 to 9.83; p = 0.001) and negatively related to the operation time (B = -21.99, 95% CI: -39.23 to -4.75; p = 0.013).Conclusion: The SFVD technique could shorten the operation time, but it would result in an increased hemoglobin drop on arrival at ICU. However, these changes did not persist postoperatively and were not mirrored in postoperative clinical outcomes.

The great saphenous vein is the most commonly used conduit in coronary artery bypass grafting; however, the high vein graft failure rates remain an unresolved issue. Here, we compared different harvesting techniques for mouse vein grafts and found that the construction of a denser lymphatic network contributed to improved vein graft patency. Dual lymphatic tracing strategies using Lyve1-CreER;R26-tdTomato/zsGreen mice uncovered a heterogeneous lymphatic network in mouse vein grafts. The anastomotic delivery of a lymphangiogenic signal, vascular endothelial growth factor-C156S, upon surgical completion promoted autologous lymphangiogenesis. The preservation of surrounding tissue led to donor-derived lymphatic remodeling dependent on PIEZO1-induced CD44 cleavage. The autologous and donor-derived lymphatic structures integrated with each other in the anastomotic area, and the loss of either component aggravated inflammation-associated neointima formation. Obesity was identified as an independent factor in mouse- and patient-derived venous samples, contributing to the perivenous macrophage accumulation and functional lymphatic remodeling, which intensified the vein graft benefits induced by surrounding tissue preservation. Collectively, this study provides both preoperative and perioperative therapeutic strategies to improve vein grafts and shows that preserving perivenous lymphatic vessels or promoting autologous lymphangiogenesis could enhance vein graft patency.

Objective: Autoimmune hepatitis (AIH) is a chronic progressive autoimmune disease with unclear etiology. As a bioactive metabolite of Vitamin D, 1,25(OH)(2)D-3 can stimulate the production of tolerogenic dendritic cells (DCs) that overexpress programmed cell death ligand 1 (PD-L1). Although these cells have been shown to play a part in autoimmune diseases, their role in AIH remains unclear. Methods: This study aimed to investigate the potential effect of 1,25(OH)(2)D-3-modulated DCs (PD-L1high VD3-DCs) in a murine model of experimental autoimmune hepatitis (EAH). Results: Our results showed that intravenous injection of PD-L1high VD3-DCs significantly attenuated liver injury and EAH severity in mice. In addition, PD-L1high VD3-DC infusion improved the imbalance between splenic regulatory T cells (TFR) and follicular helper T (TFH) cells in EAH mice by increasing the number of TFR cells and restoring TFR/TFH ratio. Also, PD-L1high VD3-DC infusion selectively promoted TFR expansion and inhibited TFH differentiation. Furthermore, PD-L1high VD3-DC infusion increased TGF-beta and IL-10 production, inhibited IL-21 secretion, upregulated key TFH transcriptional factors, and reduced the levels of serum immunoglobulins in EAH mice. Conclusions: To sum up, PD-L1high VD3-DC infusion could control EAH progression in mice by regulating TFR/TFH imbalance, indicating PD-L1high VD3-DC infusion might be a promising therapeutic approach for AIH treatment.