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Background To identify the association between tricuspid annular circumference and secondary tricuspid regurgitation and analyze the risk factors of recurrent tricuspid regurgitation after concomitant tricuspid annuloplasty during left heart surgery. Methods From October 2018 to June 2019, a total of 117 patients receiving concomitant tricuspid annuloplasty within left heart surgery were enrolled. Severity of tricuspid regurgitation was classified as 4 subtypes: normal, mild, moderate and severe. Perioperative data and mid-term outcome were collected. Tricuspid annular circumference (TAC) was measured under cardiac arrest during surgery procedure by cardioplegia. Optimal TAC and TAC index (TAC/body surface area, BSA) cutoffs of significant tricuspid annulus dilatation (moderate and severe) were obtained. Univariable and multivariable logistic regression analyses were performed to identify the risk factors of postoperative recurrent tricuspid regurgitation. The follow up period is 13–19 months (mean 15.5 ± 3.2 months). Results There was 1 patient was excluded who died after surgery. A total of 116 patients receiving tricuspid annuloplasty were included. Optimal cutoffs of significant tricuspid annulus dilatation were recommended (TAC 11.45 cm, Sensitivity 82.89%, Specificity 73.68%, AUC 0.915; TAC index 7.09 cm/m2, Sensitivity 73.68%, Specificity 85%, AUC 0.825, respectively). Based on findings of multivariable logistic regression, it has been showed that TAC index and postoperative atrial fibrillation were the independent risk factors of recurrent regurgitation after surgery. Optimal TAC index cutoff to predict recurrent tricuspid regurgitation was 7.86 cm/m2 Conclusions The severity of secondary tricuspid regurgitation is associated with the tricuspid annular circumference. The cut-offs of significant tricuspid regurgitation (more than moderate) were TAC 11.45 cm and TAC index 7.09 cm/m2, respectively. Clinically, concomitant tricuspid annuloplasty is relative safe and effective. TAC index ≥ 7.86 cm/m2 and postoperative atrial fibrillation are the risk factors of recurrent significant tricuspid regurgitation after concomitant tricuspid annuloplasty during left heart surgery.

Background Many comparative studies of percutaneous balloon mitral valvuloplasty (PBMV) and surgical mitral commissurotomy (SMC) in rheumatic mitral stenosis (MS) were done in the last few decades. With the development of valve repair techniques, various surgical rheumatic valve repair techniques have been applied in clinic, but there is a lack of comparison with PBMV. Our study was designed to compare the perioperative and mid-term outcomes of PBMV and mitral valve repair with "four-step" procedure in the treatment of rheumatic MS. Methods Patients with MS were treated with PBMV or rheumatic mitral valve repair (rMVP) at Beijing Anzhen Hospital between January 1, 2013 and September 30, 2018 were selected. By using propensity score matching (PSM) method, we compared the changes in post-operation clinical outcomes between the two matched groups. Kaplan-Meier analyses was used for survival analysis and drawing the curve, and log-rank test were used to compare intergroup differences. Results A total of 252 cases were enrolled after selection, 74 cases in PBMV and 178 cases in rMVP. Seventy-four pairs were matched successfully after PSM. There were 53 females in PBMV and 54 in rMVP. The mean age of two groups was 46.95±12.50 and 47.55±11.91 years respectively. There was no significantly differences in mitral valve orifice area (MVOA) (1.05±0.32 vs. 0.97±0.24 cm2, P=0.12) and left ventricular ejection fraction (EF) (62.36%±5.17% vs. 62.52%±4.94%, P=0.76) between two groups preoperatively. Baseline characteristics were basically balanced after PSM. In each group, there was one case transferred to surgical mitral valve replacement due to the failure of valvuloplasty before discharge. All patients survived the interventions and no severe complications were found. MVOA were significantly increased in rMVP compared with PBMV postoperatively, as well as grading of MS and tricuspid regurgitation (TR) were significantly improved in rMVP. Three cases in PBMV were lost during the follow-up. Mitral replacement was performed in 11 patients and one of them died in PBMV, while none of patients underwent re-intervention in rMVP, but one patient died of pneumonia. Conclusions For selected patients with rheumatic MS in China, our study shows that there are comparable clinical outcomes in terms of operative, mid-term mortality and complications between PBMV and surgical rMVP with "four-step" procedure. Surgical rMVP shows more advantageous in the correction of valve stenosis and the management of concomitant tricuspid valve lesions and atrial fibrillation (AF).

Many studies have shown that long-noncoding RNA (lncRNA) is associated with cardiovascular disease, but its molecular mechanism is still unclear. In this study, we explored the role of lncRNA ANRIL in ox-LDL-induced phenotypic transition of human aortic smooth muscle cells (HASMC). The results of quantitative fluorescence PCR showed that the expression of ANRIL in patients with coronary atherosclerotic heart disease (CAD) was significantly higher than that in normal subjects. RNA-FISH detection showed that the ANRIL expression increased in HASMC treated by ox-LDL. Ox-LDL could upregulate the expression of ANRIL and ROS and promote the phenotypic transition of HASMC. After downregulation of ANRIL by siRNA, ROS level decreased and HASMC phenotypic transition alleviated. ANRIL could act as a molecular scaffold to promote the binding of WDR5 and HDAC3 to form WDR5 and HDAC3 complexes, they regulated target genes such as NOX1 expression by histone modification, upregulated ROS level and promote HASMC phenotype transition. Therefore, we found a new epigenetic regulatory mechanism for phenotype transition of VSMC, ANRIL was a treatment target of occlusive vascular diseases.

We speculated that ubiquitin specific peptidase 4 (USP4) may deubiquitinate interferon regulatory factor 4 (IRF4) and affect T helper type 2 (Th2) cell function. This study aimed to validate this hypothesis. Here, the interaction between USP4 and IRF4 were analyzed by co-immunoprecipitation assay. The deubiquitin effect of USP4 on IRF4 was analyzed by the Ni-NTA pull down assay. Luciferase reporter gene constructs were used to analyze the effects of USP4, IRF4 and nuclear factor of activated T cell-2 (NFATc2) on the activation of the interleukin-4 (IL-4) promoter. Then, the Th2 cells were infected with sh-USP4 to analyze the effects of USP4 on the expression levels of IRF4 and Th2-related cytokines. Western blotting and RT-qPCR were used to detect the protein and mRNA expression levels, respectively. To determine the levels of IL-4 and IRF4 in rheumatic heart disease (RHD) patients, peripheral blood mononuclear cells (PBMCs) were separated by density gradient centrifugation from RHD patients and healthy controls, and flow cytometric analysis was performed. Our results validated the interaction between USP4 and IRF4, and effects of USP4 on stabilization and deubiquitination of IRF4 were also found. Importantly, USP4 and IRF4 synergized with NFATc2 to specifically enhance NFAT-mediated activation of the IL-4 promoter. USP4 knockdown not only decreased the expression level of IRF4, but also affected the expression level of Th2-related cytokines. Finally, the increased level of IL-4 and IRF4 in PBMCs of RHD patients were observed. On the whole, our data indicate that USP4 interacts with and deubiquitinates IRF4, and also stabilizes IRF4 protein and promotes IRF4 function to facilitate IL-4 expression in Th2 cells, which may be related to the pathological process of RHD.