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Background: Atrial fibrillation (AF) recurrence after ablation will increase mortality and morbidity during follow up. We attempted to evaluate the relationship between circular RNAs (circRNA) and AF recurrence to establish a predictive model for early intervention. Methods: Patients who received surgical ablation retrospectively were analyzed. The expression of circRNAs were detected in the left atrial appendage. The independent risk factors of late recurrence were analyzed by multivariate analysis. The predictive model was visualized by Nomogram and tested by receiver operating characteristic curve and calibration plot. Kaplan-Meier plot was used to compare the rate of freedom from AF recurrence after surgery. The relationships between circRNAs and clinical characteristics were detected by Spearman’s correlation analysis. Results: A total of 136 patients were enrolled from September 2018 to June 2019, 55 patients experienced late recurrence during one-year follow up. Increased age, longer AF duration and increased circ 81906-RYR2, circ 44782-LAMA2, circ 418-KCNN2 and circ 35880-ANO5 were detected in recurrent patients. Multivariate analysis revealed that increased age (odds ratio (OR)=1.072, P = 0.006), longer AF duration (OR=1.007, P = 0.036) and increased circ 81906-RYR2 (OR=2.210, P < 0.001) were independent risk factors for late recurrence. Area under the curve was 0.77, and the cut-off value was 70 points of the predictive model. Kaplan-Meier plots showed that patients over 70 points tended to experience AF recurrence. Conclusion: Circ 81906-RYR2 could be a new predictor of late recurrence after surgical ablation. A predictive model consists of age, atrial fibrillation duration, and circ 81906-RYR2 was alternative for early intervention of AF recurrence.

Objective: Repair or replacement remains debatable in rheumatic heart disease. To regain optimal mean transvalvular pressure gradients and end-diastolic peak flow velocity, the modified release technique combined peeling in the anterior leaflet and separated the shortened chordal. In the end, the mid and long-term outcomes of the modified release technique were evaluated. Methods: We retrospectively analyzed a series of 128 patients with rheumatic mitral stenosis, from January 2018 to July 2021 in our center. All patients undergoing mitral valve repair were using the modified release technique. The effect of mitral valve repair was evaluated by intraoperative transesophageal echocardiography and postoperative transthoracic echocardiography. Results: All the 128 patients successfully repaired the mitral valve. The intraoperative transesophageal echocardiography showed trivial or mild regurgitation. The aortic valve was repaired without obvious regurgitation in 12 cases, 5 cases received an aortic valve replacement, 89 cases underwent tricuspid annuloplasty. There were no blood transfusions in most patients, no deaths nor complications during peri-operation, also, no deaths and adverse events were observed during the follow-up period from 3 to 42 months. During the follow-up, 122 cases had no mitral valve regurgitation and 2 cases of moderate regurgitation, 4 cases of mild to moderate regurgitation. The mean peak flow velocity was 1.2 ± 0.3 m / s, no new-onset stenosis occurred. Conclusion: Modified release technique is safe and feasible. Its durability is acceptable in the long-term, with no new-onset stenosis during the follow-up.

Objective: Ventricular septal defect (VSD) induced by acute myocardial infarction (AMI) is rare but lethal, with high mortality even after surgical repair. Our aim was to assess the association between the time interval and surgical repair effects in patients with VSD following AMI. Methods: From January 2003 to December 2017, 14 patients with VSD induced by AMI received surgical therapy in our department. We retrospectively reviewed the patients’ clinical manifestations, surgical methods, and outcomes. According to the time interval from AMI onset and surgery, we divided the patients into two groups: Group 1 (N = 9), more than one week, and Group 2 (N = 5), less than one week. A comparison study was performed, and differences were analyzed. Results: The mean age of the entire group was 65.5±3.3 years, with 78.6% males (11/14). VSDs were anterior apical in 10 (71.4%) and posterior inferior in 4 (28.6%) patients. The average size of the VSD was 15.8±5.8 mm. Compared with Group 1, Group 2 had poorer left ventricular function (LVEF 40.8±10.3% vs. 30.4±2.3%, P = 0.035) and a higher rate of urgent procedures (11.1% vs. 100.0%, P = 0.003). The mortality rate was 14.3% (2/14). Mechanical support was more common in Group 2 than Group 1. No resistant shunt or death was found during follow up. Conclusions: VSD following AMI is safer for more than one week, but surgical treatment is also acceptable for patients requiring urgent surgery due to hemodynamic instability. Mechanical assistive devices can improve the perioperative success rate.

Background and aims Atherosclerosis (AS) is the leading cause of cardiovascular diseases. PGC-1α is a key regulator of cellular energy homeostasis, but its role in AS remains debatable. Methods and results In our study, PGC-1α was shown to be significantly decreased in the media of human atherosclerotic vessels. To explore whether miRNAs might be regulated by PGC-1α in vascular smooth muscle cells (VSMCs), microarray analysis was performed. Microarray and Pearson's correlation analysis showed that PGC-1α and miR-378a were positively correlated in vivo and in vitro. As an upstream co-activator, PGC-1α was found to regulate miR-378a through binding to the transcriptional factor NRF1 in VSMCs. Therefore, the decreased expression of PGC-1α might account for suppression of miR-378a in VSMCs in AS. Furthermore, IGF1 and TLR8, two genes known to be aberrantly up-regulated in atherogenic vessels, were identified as direct targets of miR-378a. In vitro up-regulation of miR-378a markedly inhibited free fatty acid (FFA)-induced VSMC proliferation, migration and inflammation through targeting IGF1 and TLR8. Conclusions These findings highlight the protective role of the PGC-1α/NRF1/miR-378a regulatory axis in AS progression and suggest miR-378a as potential therapeutic target for AS treatment.

Mitral valve repair for extensive commissural prolapse is complex; several methods have been reported with variable results. To restore the leaflet area, we introduced an innovative and effective method rather than a simple folding technique through reconstructing a neocommissure with a "collar-like" plasty technique.From 2016 to 2021, 62 patients with mitral valve extensive commissural prolapse that received the "collar-like" plasty technique were included.The mean age was 51.7 ± 13.8 years, and 38 (61%) were female. Postplasty transesophageal echocardiography showed the mean transvalvular pressure gradients were 3.8 ± 1.2 mm Hg, end diastolic peak flow velocity was 1.1 ± 0.3 m/s, and coaptation height was 7.9 ± 1.1 mm. During the follow-up period of 3 to 6 months, no deaths or cardiovascular-/valvular plasty-related adverse events occurred. All patients regained their heart function and returned to normal physical activities.The "collar-like" plasty technique can be safely performed for patients with extensive commissural prolapse. Echocardiography revealed that the technique can restore the leaflet area of low transvalvular pressure and flow velocity.

Rationale: Targeting vascular smooth muscle cell (VSMC) phenotypic switching is a promising therapeutic approach for atherosclerosis. Dysregulation of PGC1α (peroxisome proliferator-activated receptor gamma, coactivator 1α), a key regulator of cellular energy metabolism, has been implicated in the pathogenesis of atherosclerosis, yet its role in atherosclerosis remains controversial. Objective: The current study aimed to determine whether and how PGC1α in VSMCs regulates atherosclerosis progression. Methods and Results: We generated transgenic rabbits with SMC-specific PGC1α overexpression and showed that these rabbits developed significantly less aortic atherosclerosis than their nontransgenic littermates after high-cholesterol diet feeding, while total plasma cholesterol levels were similar. As indicated by the restored expression of VSMC differentiation marker genes, the high-cholesterol diet-induced phenotypic switching in the aortic media was largely reversed in transgenic rabbits, accompanied by decreased levels of synthetic phenotype genes, proinflammatory cytokines, adhesion molecules, macrophage infiltration, MMPs (matrix metalloproteinases), reactive oxygen species production and senescence. Ex vivo studies further showed that VSMC-specific PGC1α overexpression markedly suppressed the promotive effect of high-cholesterol diet feeding on the association of SRF (serum response factor) with ELK1 (ETS transcription factor ELK1), a TCF (ternary complex factor) that acts as a myogenic repressor in VSMCs, thereby preserving the VSMC contractile phenotype. Furthermore, knockdown of PGC1α remarkably increased ERK (extracellular signal-regulated kinase)1/2-ELK-1 signaling, which promoted phenotypic switching and proliferation of cultured rabbit VSMCs. In addition, we showed that PGC1α can regulate EGFR (epidermal growth factor receptor)-ERK1/2 MAPK (mitogen-activated protein kinase) signaling via modulating PPARγ (peroxisome proliferator-activated receptor γ) activity in RVSMCs (rabbit vascular smooth muscle cells). Finally, we showed that these beneficial results of SMC-specific PGC1α overexpression can be extrapolated from rabbits to human VSMCs and clinical settings. Conclusions: We demonstrated a critical role of PGC1α in maintaining the contractile phenotype of VSMCs and highlighted the therapeutic potential of PGC1α for atherosclerosis.

The global rise in obesity has become a public health crisis. During the onset of obesity, disrupted catecholamine signals have been described to contribute to excess fat accumulation, however, the molecular and metabolic change of subcutaneous adipose tissue (SAT) upon chronic high-fat feeding has rarely been investigated. Here, we show that chronic high-fat feeding caused a significant decrease in the expression of thermogenic genes and acquisition of partial deleterious features of visceral fat in SAT. Upregulated miR-149-3p was involved in this obesity-induced “visceralization” of SAT via inhibiting PRDM16, a master regulator that promoted SAT thermogenesis. Reduction of miR-149-3p significantly increased PRDM16 expression in SAT, with improved whole-body insulin sensitivity, decreased SAT inflammation, and liver steatosis in high-fat fed mice. These findings provided direct evidence of the anti-obese and anti-diabetic effect of PRDM16 in the obese background for the first time and identified that miR-149-3p could serve as a therapeutic target to protect against diet-induced obesity and metabolic dysfunctions. Keywords: diet-induced obesity, miR-149-3p, Prdm16, subcutaneous adipose tissue, thermogenesis

Background: Acute Stanford type A aortic dissection (ATAAD) is often misdiagnosed as an acute coronary syndrome (ACS), and antiplatelet therapy (APT) for ACS will influence the timing and outcome of ATAAD. We reviewed the surgical outcome of these misdiagnosed ATAAD patients. Methods: From January 2011 to December 2015, 309 ATAAD patients received surgical therapy in our department, among whom 15 patients were misdiagnosed as ACS and took oral APT. We retrospectively reviewed the data of the perioperative and follow-up period. Results: The average age of these 15 patients was 60.6±8.7 years old (9 males, 6 females). Five patients took aspirin orally, and 10 took aspirin and clopidogrel. Operations were performed 7, 3, and 1 day after stopping the agents in 2, 3, and 1 patient, respectively; the other 5 patients received emergency operation without stopping the agents. The cardiopulmonary bypass (CPB) time was 259.7±64.8 minutes, aortic cross-clamp time was 181.0±51.7 minutes, and selective cerebral perfusion and lower body arrest time were 34.9± 8.1 minutes. There were two in-hospital deaths due to circulation failure (mortality 13.3%). The average drainage volume in the first 24 h after operation was 800.7±598.8 mL. During a mean follow-up period of 20.6±17.4 months, one patient had a sudden death. Conclusions: ATAAD misdiagnosed as ACS is not rare, and APT will increase the risk of bleeding in ATAAD patients. The decision of operation time relies on considering the balance between the rupture risk of aortic dissection and the hemorrhage risk of APT. The emergency operation for these patients will increase bleeding and transfusion.

Ebstein's anomaly (EA) is a rare but difficult to manage congenital heart disease with a wide spectrum of clinical manifestations. We present a simplified repair method which combines the plication of the atrialized right ventricle, tricuspid leaflet repair and ring annuloplasty. This method is suitable for older adult EA patients with progressive right heart dysfunction symptoms. Compared with complex repair methods (such as Cone reconstruction) this simplified repair method can reduce surgical risk, and achieve mild or less tricuspid regurgitation with acceptable long-term effects compared with prosthetic valve replacement.

Background: Atrial fibrillation recurrence after surgical ablation in valvular atrial fibrillation patients will increase the mortality and morbidity during follow-up. In this study, we attempted to evaluate the relationship between circular RNAs in left atrial appendage and atrial fibrillation recurrence to establish a predictive model for early intervention.Methods: A retrospective case control study of all patients who underwent surgical ablation during valve surgery was performed. The expression level of circular RNAs were detected in the left atrial appendage tissue after surgery. 24 hours Holter examination was used to evaluate the status of heart rhythm during follow-up. The independent risk factors of atrial fibrillation recurrence were analyzed by multivariate analysis. The predictive model of atrial fibrillation recurrence was visualized by Nomogram and was tested by receiver operating characteristic curve analysis. Kaplan-Meier analysis was performed to compare the rate of freedom from atrial fibrillation recurrence after surgery.Results: A total of 136 patients completed the research strategy from September 2018 to June 2019, 81 (59.6%) patients restored sinus rhythm and 55 (40.4%) patients experienced atrial fibrillation recurrence. Increased age (P=0.002), longer AF duration (Pcirc 81906-RYR2 (Pcirc 44782-LAMA2 (P=0.002), circ 418-KCNN2 (P=0.011) and circ 35880-ANO5 (Pcirc 81906-RYR2 (odd ratio=2.210, PConclusions: Circ 81906-RYR2 could be a new predictor of atrial fibrillation recurrence after surgical ablation. A predictive model consists of age, atrial fibrillation duration and expression of circ 81906-RYR2 was alternative for early intervention of atrial fibrillation recurrence.Trial registration: Retrospectively registered.

MicroRNAs have become the spotlight of the biological community for more than a decade, but we are only now beginning to understand their functions. The detection of stably expressed endogenous microRNAs in human blood suggests that these circulating miRNAs can mediate intercellular communication. Our previous study reported the surprising finding that exogenous rice MIR168a could regulate liver low-density lipoprotein receptor adapter protein 1 (LDLRAP1) gene expression in mice. Here, we show that plant MIR156a, which is abundantly expressed in dietary green veggies, also stably presents in healthy human serum. Compared with age-matched individuals, decreased levels of MIR156a are observed both in serum and blood vessel of cardiovascular disease (CVD) patients. In vitro studies demonstrate that MIR156a can directly target the junction adhesion molecule-A (JAM-A), which is up-regulated in atherosclerotic lesions from CVD patients. Functional studies show that ectopic expression of MIR156a in human aortic endothelial cells reduces inflammatory cytokine-induced monocytes adhesion by suppressing JAM-A. These findings offer a novel vasoprotective molecular mechanism of green veggies through plant microRNAs.

Background Retrospective compared the results of root reconstruction and root replacement for acute type A aortic dissection (ATAAD) patients and observed the rate of aortic insufficiency (AI) and aortic root dilation in the midterm follow-up period. Methods From 2008-2016, 427 ATAAD patients received surgical therapy in our center. There were 328 male and 99 female patients, aging from 22 to 83 years with a mean age of (51.1±12.5) years. These patients were divided into two major groups: 298 cases with root reinforcement reconstruction (Root Reconstruction), 129 cases with Bentall procedure (Root Replacement). Results The 30-day mortality was 7.7% (33/427), while no difference between the 2 procedures (8.1% and 7.0%, P=0.844). Cross-clamp, cardiopulmonary bypass, and circulatory arrest times of all the patients were 252.5±78.1, 173.6±68.9, 30.7±9.5 minutes, respectively. In the average follow-up time of (34.5±26.1) months, midterm survival rates were similar between the 2 procedures (86.2% and 86.0%, P=0.957). Only one patient received redo Bentall procedure because of severe aortic regurgitation and dilated aortic root (50 mm) in the Root Reconstruction Group. Conclusions The indication of root management of ATAAD is based on the diameter of aortic root, structure of aortic root, and the dissection involvement. For most ATAAD patients, aortic root reinforcement reconstruction is a feasible and safe method.

Early and convenient diagnosis is urgently needed for acute Stanford type A aortic dissection (AAAD) patients due to its high mortality within the first 48 hours. Circulating microRNAs (miRNAs) are promising biomarkers of cardiovascular diseases, however, little is known about circulating miRNAs involved in AAAD. Here, the blood serum was sampled from 104 AAAD+ patients and 103 age-matched donors. Initial screening was conducted using the TaqMan Low Density Array followed by RT-qPCR confirmation. According to the two-phase selection and validation process, we found that miR-25, miR-29a and miR-155 were significantly elevated, while miR-26b was markedly decreased in AAAD+ serum samples compared with AAAD− individuals. Most importantly, for individuals with hypertension, which is a major contributor to AAAD, the 4-miRNA panel also showed high accuracy in predicting those who are more likely to develop AAAD. In the blind trial set, the panel correctly classified 93.33% AAAD+ patients and 86.67% controls from the hypertension cohort. Finally, the serum miRNA-based biomarker for early AAAD detection was supported by a retrospective analysis. Taken together, we identify a distinct profile of 4-miRNA that can serve as a noninvasive biomarker for AAAD diagnosis, especially for those with hypertension.