Oesophago-pericardial fistula after catheter ablation of atrial fibrillation: a case report.

Background: Oesophageal fistula is a rare complication of catheter ablation of atrial fibrillation with most fistulas being atrio-oesophageal fistulas, but oesophageal-pericardial fistula can also happen in the absence of atrial perforation. Case summary: A 68-year-old male patient presented with chest pain 10 days after catheter ablation of paroxysmal atrial fibrillation. He was discharged after an initial negative workup that included a CT chest without contrast. He later presented again with severe chest pain and fever and was found to have an oesophageal-pericardial fistula. He underwent surgical and endoscopic treatment with good recovery. Discussion: Patients with oesophago-pericardial fistulas often have delayed presentation 1-4 weeks after the ablation procedure. Early diagnosis can be challenging. CT with oral and intravenous contrast is often used for diagnosis. Treatment often includes antibiotics, surgical or interventional drainage of infected spaces with oesophageal repair, clipping or stenting. In contrast to atrio-oesophageal fistulas that carry a high mortality rate, mortality for oesophago-pericardial fistulas appears to be much lower.

Adjunctive Right Atrial Ablation for Persistent Atrial Fibrillation With Right Atrial Enlargement: A Pilot Study.

BACKGROUND: Persistent atrial fibrillation (PerAF) is often associated with right atrial (RA) enlargement. We investigated the efficacy of RA intervention in patients with PerAF and RA enlargement. METHODS: Patients with PerAF and RA enlargement were randomised (1:1) to receive adjunctive RA ablation (left atrial [LA] + RA group; n = 60) or to receive LA ablation alone (LA-only group; n = 60). In the LA + RA group, RA ablation was performed if LA ablation failed to terminate AF. The primary end point was freedom from AF/atrial tachycardia (AT) recurrence at 12 months after a single ablation procedure without antiarrhythmic drug therapy. RESULTS: In the LA + RA group, 40 patients (67%) required RA ablation. The LA + RA group had a higher rate of acute AF termination than the LA-only group (63.3% vs 36.7%; P = 0.003). At the end of 12-month follow-up, 42 patients (70%) in the LA + RA group were free of AF/AT recurrence, compared with 31 (51.7%) in the LA-only group (log rank P = 0.034; hazard ratio 0.549, 95% confidence interval 0.310-0.974). The rate of freedom from AF recurrence was also higher in the LA + RA group than in the LA-only group (81.7% vs 63.3%; log rank P = 0.019). The 2 groups had similar rates of adverse events (5% vs 3.3%; P = 0.648). CONCLUSIONS: Adjunctive RA ablation increased the success rate of a single ablation in patients with PerAF and RA enlargement. CHINESE CLINICAL TRIAL REGISTRATION: ChiCTR220056844.

Inverse-designed counter-tapered coupler based broadband and compact silicon mode multiplexer/demultiplexer.

A mode multiplexer/demultiplexer (MUX/DeMUX) is a crucial component for constructing mode-division multiplexing (MDM) systems. In this paper, we propose and experimentally demonstrate a wide-bandwidth and highly-integrated mode MUX/DeMUX based on an inverse-designed counter-tapered coupler. By introducing a functional region composed of subunits, efficient mode conversion and evolution can be achieved, greatly improving the mode conversion efficiency. The optimized mode MUX/DeMUX has a size of only 4 µm × 2.2 µm. An MDM-link consisting of a mode MUX and a mode DeMUX was fabricated on the silicon-on-insulator (SOI) platform. The experimental results show that the 3-dB bandwidth of the TE fundamental mode and first-order mode can reach 116 nm and 138 nm, respectively. The proposed mode MUX/DeMUX is scalable and could provide a feasible solution for constructing high-performance MDM systems.

Design and experimental demonstration of a silicon five-mode (de)multiplexer based on multi-phase matching condition.

A compact 5-mode (de)multiplexer [(De)MUX] is proposed and experimentally demonstrated based on the principle of multi-phase matching. The proposed device comprises a cascaded asymmetric directional coupler (ADC) based on 3-mode phase-matching, a polarization beam combiner, and a taper waveguide connecting them. The multiple modes in the access waveguides are matched to different modes in the same bus waveguide, which eliminates the need for additional taper structures and results in a total coupling length of only 18.9 µm. Experimental results exhibit that the insertion losses of the five modes are below 3.4 dB, and the mode crosstalks are below -15 dB at the central wavelength. The 3-dB bandwidths of TM0, TM1, TE0, TE1, and TE2 modes are greater than 100 nm, 46 nm, 100 nm, 28 nm, and 37 nm, respectively. The proposed device can serve as a key functional component in highly integrated on-chip mode-division multiplexing systems.

Quercetin improves cerebral ischemia/reperfusion injury by promoting microglia/macrophages M2 polarization via regulating PI3K/Akt/NF-κB signaling pathway.

The modulation of microglial polarization from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype shows promise as a therapeutic strategy for ischemic stroke. Quercetin, a natural flavonoid abundant in various plants, possesses anti-inflammatory, anti-apoptotic, and antioxidant properties. Nevertheless, its effect and underlying mechanism on microglia/macrophages M1/M2 polarization in the treatment of cerebral ischemia/reperfusion injury (CI/RI) remain poorly explored. In the current study, we observed that quercetin ameliorated neurological deficits, reduced infarct volume, decreased the number of M1 microglia/macrophages (CD16/32+/Iba1+), and enhanced the number of M2 microglia/macrophages (CD206+/Iba1+) after establishing the CI/RI model in rats. Subsequent in vivo and in vitro experiments indicated that quercetin downregulated M1 markers (CD86, iNOS, TNF-α, IL-1ß, and IL-6) and upregulated M2 markers (CD206, Arg-1, IL-10, and TGF-ß). Network pharmacology analysis and molecular docking revealed that the PI3K/Akt/NF-κB signaling pathway emerged as the core pathway. Western blot confirmed that quercetin upregulated the phosphorylation of PI3K and Akt, while alleviating the phosphorylation of IκBα and NF-κB both in vivo and in vitro. However, the PI3K inhibitor LY294002 reversed the effects of quercetin on M2 polarization and the expression of key proteins in the PI3K/Akt/NF-κB pathway in primary microglia after oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro. Collectively, our findings demonstrate that quercetin facilitates microglia/macrophages M2 polarization by modulating the PI3K/Akt/NF-κB signaling pathway in the treatment of CI/RI. These findings provide novel insights into the therapeutic mechanisms of quercetin in ischemic stroke.

Discovery of TBX20 as a Novel Gene Underlying Atrial Fibrillation.

Atrial fibrillation (AF), the most prevalent type of sustained cardiac dysrhythmia globally, confers strikingly enhanced risks for cognitive dysfunction, stroke, chronic cardiac failure, and sudden cardiovascular demise. Aggregating studies underscore the crucial roles of inherited determinants in the occurrence and perpetuation of AF. However, due to conspicuous genetic heterogeneity, the inherited defects accounting for AF remain largely indefinite. Here, via whole-genome genotyping with genetic markers and a linkage assay in a family suffering from AF, a new AF-causative locus was located at human chromosome 7p14.2-p14.3, a ~4.89 cM (~4.43-Mb) interval between the markers D7S526 and D7S2250. An exome-wide sequencing assay unveiled that, at the defined locus, the mutation in the TBX20 gene, NM_001077653.2: c.695A>G; p.(His232Arg), was solely co-segregated with AF in the family. Additionally, a Sanger sequencing assay of TBX20 in another family suffering from AF uncovered a novel mutation, NM_001077653.2: c.862G>C; p.(Asp288His). Neither of the two mutations were observed in 600 unrelated control individuals. Functional investigations demonstrated that the two mutations both significantly reduced the transactivation of the target gene KCNH2 (a well-established AF-causing gene) and the ability to bind the promoter of KCNH2, while they had no effect on the nuclear distribution of TBX20. Conclusively, these findings reveal a new AF-causative locus at human chromosome 7p14.2-p14.3 and strongly indicate TBX20 as a novel AF-predisposing gene, shedding light on the mechanism underlying AF and suggesting clinical significance for the allele-specific treatment of AF patients.

MiR-199a-5p enhances neuronal differentiation of neural stem cells and promotes neurogenesis by targeting Cav-1 after cerebral ischemia.

AIMS: MicroRNAs (miRs) are involved in endogenous neurogenesis, enhancing of which has been regarded as a potential therapeutic strategy for ischemic stroke treatment; however, whether miR-199a-5p mediates postischemic neurogenesis remains unclear. This study aims to investigate the proneurogenesis effects of miR-199a-5p and its possible mechanism after ischemic stroke. METHODS: Neural stem cells (NSCs) were transfected using Lipofectamine 3000 reagent, and the differentiation of NSCs was evaluated by immunofluorescence and Western blotting. Dual-luciferase reporter assay was performed to verify the target gene of miR-199a-5p. MiR-199a-5p agomir/antagomir were injected intracerebroventricularly. The sensorimotor functions were evaluated by neurobehavioral tests, infarct volume was measured by toluidine blue staining, neurogenesis was detected by immunofluorescence assay, and the protein levels of neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), caveolin-1 (Cav-1), vascular endothelial growth factor (VEGF), and brain-derived neurotrophic factor (BDNF) were measured by Western blotting. RESULTS: MiR-199a-5p mimic enhanced neuronal differentiation and inhibited astrocyte differentiation of NSCs, while a miR-199a-5p inhibitor induced the opposite effects, which can be reversed by Cav-1 siRNA. Cav-1 was through the dual-luciferase reporter assay confirmed as a target gene of miR-199a-5p. miR-199a-5p agomir in rat stroke models manifested multiple benefits, such as improving neurological deficits, reducing infarct volume, promoting neurogenesis, inhibiting Cav-1, and increasing VEGF and BDNF, which was reversed by the miR-199a-5p antagomir. CONCLUSION: MiR-199a-5p may target and inhibit Cav-1 to enhance neurogenesis and thus promote functional recovery after cerebral ischemia. These findings indicate that miR-199a-5p is a promising target for the treatment of ischemic stroke.

Multi-centre, prospective randomized comparison of three different substrate ablation strategies for persistent atrial fibrillation.

AIMS: The optimal strategy for persistent atrial fibrillation (PerAF) is poorly defined. We conducted a multicentre, randomized, prospective trial to compare the outcomes of different ablation strategies for PerAF. METHODS AND RESULTS: We enrolled 450 patients and randomly assigned them in a 1:1:1 ratio to undergo pulmonary vein isolation and subsequently undergo the following three different ablation strategies: anatomical guided ablation (ANAT group, n = 150), electrogram guided ablation (EGM group, n = 150), and extensive electro-anatomical guided ablation (EXT group, n = 150). The primary endpoint was freedom from atrial fibrillation (AF) lasting longer than 30 s at 12 months after a single ablation procedure. After 12 months of follow-up, 72% (108) of patients in the EXT group were free from AF recurrence, as compared with the 64% (96) in the EGM group (P = 0.116), and 54% (81) in the ANAT group (P = 0.002). The EXT group showed less AF/atrial tachycardia recurrence than the EGM group (60% vs. 50%, P = 0.064) and the ANAT group (60% vs. 37.3%, P < 0.001). The EXT group showed the highest rate of AF termination (66.7%), followed by 56.7% in the EGM group, and 20.7% in the ANAT group. The AF termination signified less AF recurrence at 12 months compared to patients without AF termination (30.1% vs. 42.7%, P = 0.008). Safety endpoints did not differ significantly between the three groups (P = 0.924). CONCLUSIONS: Electro-anatomical guided ablation achieved the most favourable outcomes among the three ablation strategies. The AF termination is a reliable ablation endpoint.

Temporal and Spatial Changes of Proarrhythmic Substrate in Premature Ventricular Contraction-Induced Cardiomyopathy.

BACKGROUND: The changes in proarrhythmic substrates and malignant ventricular arrhythmia mechanisms caused by premature ventricular contraction-induced cardiomyopathy (PVCCM) remain unclear. OBJECTIVES: The goal of this study was to establish the electrophysiological mechanism of how high-load PVC causes malignant arrhythmia. METHODS: Thirteen swine were exposed to 50% paced PVC from the right ventricular apex for 12 weeks (PVCCM, n = 6) and no pacing for 12 weeks (control, n = 7). Cardiac function was quantified biweekly with echocardiography. Computed tomography scans and electrophysiological examinations were performed monthly to dynamically evaluate the changes in the cardiac structure and the arrhythmogenic substrate. RESULTS: The decreases in the cardiac function and ventricular enlargement in the PVCCM group were significant after 12 weeks of PVC stimulation compared with the control group (P < 0.001). Electrophysiological examination found that the ventricular effective refractory period dispersion (0.071 ± 0.008), area of the low-voltage zone (9.41 ± 1.55 cm2), and malignant ventricular arrhythmia inducibility (33.3%) of the PVCCM group increased significantly at week 8 after pacing (P < 0.001 vs the control group); these changes slowed down after 8 weeks. Moreover, the distribution of the low-voltage zone presented obvious spatial heterogeneity, especially in the anterior wall of the right ventricle, accompanied by delayed activation in the sinus rhythm (67 ± 13 milliseconds). Consistently, the proportion of ventricular fibrosis- and expression-related proteins were significantly increased in the PVCCM group (P < 0.001), especially in the right ventricle. Moreover, proteomic analysis confirmed the spatial profile of these fibrotic changes in the PVCCM group. CONCLUSIONS: High-burden PVC can cause significant temporal and spatial heterogeneity changes in proarrhythmic substrates, which are potentially related to the upregulation of calcium signaling caused by asynchronous activation.

Rotor mechanism and its mapping in atrial fibrillation.

Treatment of atrial fibrillation (AF) remains challenging despite significant progress in understanding its underlying mechanisms. The first detailed, quantitative theory of functional re-entry, the 'leading circle' model, was developed more than 40 years ago. Subsequently, in decades of study, an alternative paradigm based on spiral waves has long been postulated to drive AF. The rotor as a 'spiral wave generator' is a curved 'vortex' formed by spin motion in the two-dimensional plane, identified using advanced mapping methods in experimental and clinical AF. However, it is challenging to achieve complementary results between experimental results and clinical studies due to the limitation in research methods and the complexity of the rotor mechanism. Here, we review knowledge garnered over decades on generation, electrophysiological properties, and three-dimensional (3D) structure diversity of the rotor mechanism and make a comparison among recent clinical approaches to identify rotors. Although initial studies of rotor ablation at many independent centres have achieved promising results, some inconclusive outcomes exist in others. We propose that the clinical rotor identification might be substantially influenced by (i) non-identical surface activation patterns, which resulted from a diverse 3D form of scroll wave, and (ii) inadequate resolution of mapping techniques. With rapidly advancing theoretical and technological developments, future work is required to resolve clinically relevant limitations in current basic and clinical research methodology, translate from one to the other, and resolve available mapping techniques.

A novel approach for quantitative electrogram analysis for driver identification: Implications for ablation in persistent atrial fibrillation.

Objective: This study sought to study the feasibility, efficacy, and safety of using multiscale entropy (MSE) analysis to guide catheter ablation for persistent atrial fibrillation (PsAF) and predict ablation outcomes. Methods: We prospectively enrolled 108 patients undergoing initial ablation for PsAF. MSE was calculated based on bipolar intracardiac electrograms (iEGMs) to measure the dynamical complexity of biological signals. The iEGMs data were exported after pulmonary vein isolation (PVI), then calculated in a customed platform, and finally re-annotated into the CARTO system. After PVI, regions of the highest mean MSE (mMSE) values were ablated in descending order until AF termination, or three areas had been ablated. Results: Baseline characteristics were evenly distributed between the AF termination (n = 38, 35.19%) and the non-termination group. The RA-to-LA mean MSE (mMSE) gradient demonstrated a positive gradient in the non-termination group and a negative gradient in the termination group (0.105 ± 0.180 vs. -0.235 ± 0.256, P < 0.001). During a 12-month follow-up, 29 patients (26.9%) had arrhythmia recurrence after single ablation, and 18 of them had AF (62.1%). The termination group had lower rates of arrhythmia recurrence (15.79 vs. 32.86%, Log-Rank P = 0.053) and AF recurrence (10.53 vs. 20%, Log-Rank P = 0.173) after single ablation and a lower rate of arrhythmia recurrence (7.89 vs. 27.14%, Log-Rank P = 0.018) after repeated ablation. Correspondingly, subjects with negative RA-to-LA mMSE gradient had lower incidences of arrhythmia (16.67 vs. 35%, Log-Rank P = 0.028) and AF (16.67 vs. 35%, Log-Rank P = 0.032) recurrence after single ablation and arrhythmia recurrence after repeated ablation (12.5 vs. 26.67%, Log-Rank P = 0.062). Marginal peri-procedural safety outcomes were observed. Conclusion: MSE analysis-guided driver ablation in addition to PVI for PsAF could be feasible, efficient, and safe. An RA < LA mMSE gradient before ablation could predict freedom from arrhythmia. The RA-LA MSE gradient could be useful for guiding ablation strategy selection.

The nonlinear association between HbA1c and cognitive impairment in patients with alcohol use disorder.

Background: Extensive research has indicated that higher levels of glycated hemoglobin (HbA1c) are associated with poor cognitive performance regardless of the presence of diabetes. To our knowledge, the association between HbA1c levels and cognitive decline in patients with alcohol use disorder is not well understood. This study aimed to investigate whether HbA1c was associated with cognitive impairment in patients with alcohol use disorder. Methods: Patients admitted to the Psychiatry Department of the Third Hospital of Quzhou with a confirmed diagnosis of alcohol-related cognitive impairment were recruited between January 2019 and February 2022. Their HbA1c levels were measured, and they completed the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) after at least one week of monitored abstinence from alcohol. Univariate linear regression, multivariate linear regression and generalized additive models (GAMs) were used to investigate the association of HbA1c with MMSE and MoCA scores. Results: In total, 227 patients were included. Univariate and multivariate regression analyses suggested that HbA1c was negatively associated with MMSE and MoCA scores after adjustment for potential confounders (P < 0.05). The GAM analysis revealed that the relationships between the HbA1c level and the MMSE and MoCA scores were bell-shaped. The inflection points were 5.3% and 5.2% for the MMSE and MoCA respectively. Conclusion: The results of this study suggest that HbA1c levels are significantly related to cognitive impairment in patients with alcohol use disorder. Future studies are required to determine the effects of optimal glucose control in people with alcohol use disorder.

Recent advances in metal-organic frameworks for gas adsorption/separation.

The unique structural advantage of metal-organic frameworks (MOFs) determines the great prospect and developability in gas adsorption and separation. Both ligand design and microporous engineering based on crystal structure are significant lever for coping with new application exploration and requirements. Focusing on the designable pore and modifiable frameworks of MOFs, this review discussed the recent advances in the field of gas adsorption and separation, and analyzed the host-guest interaction, structure-performance relations, and the adsorption/separation mechanism from ligand design, skeleton optimization, metal node regulation, and active sites construction. Based on the function-oriented perspective, we summarized the main research recently, and made an outlook based on the focus of microporous MOFs that require further attention in the structure design and industrial application.

Prognostic impact of blood urea nitrogen/creatinine ratio changes in patients with acute ischemic stroke.

BACKGROUND: Blood urea nitrogen (BUN)/creatinine (Cr) ratio was an independent predictor of stroke-in-evolution (SIE) among patients who had suffered an acute ischemic stroke. We investigated the association of changes in BUN/Cr on stroke outcome during hospitalization after acute ischemic stroke (AIS). METHODS: AIS patients admitted within 3 days from stroke onset (2020-2021) were included in the study. Baseline data, including BUN and Cr levels, were collected. Univariate linear regression and a multivariate regression model were applied to assess the relationship between the change of BUN/Cr and short-term outcomes. RESULTS: One hundred and eighty-one patients were included. The mean increase of BUN/Cr level was - 2.0 ± 1.78. Univariate linear regression suggested that baseline NIHSS, thrombolysis, change of BUN/Cr, and history of atrial fibrillation, statin use, and antiplatelet therapy was associated with the decrease in NIHSS during hospitalization (P < 0.05). After adjusting for potential confounders, multivariate regression analysis revealed the associations between the decrease in BUN/Cr and favorable outcome are significant (ß = 0.21, 95% CI = 0.14,-0.28). CONCLUSION: The decrease in BUN/Cr is positively correlated with a better early neurological improvement in AIS patients.

Right atrial appendage: an important structure to drive atrial fibrillation.

PURPOSE: Understanding of the atrial fibrillation (AF) driven by right atrial appendage (RAA) is limited. This study aimed to understand the characteristics of the AF driven by RAA and explore ablation methods. METHODS: This was a retrospective study and patients who were identified as having the AF driven by RAA were reviewed. Ablation was performed during AF. Potential maps of the left and right atrium, electrophysiological examinations, and ablation methods were studied. RESULTS: Among the 20 identified patients (mean age 67.0 ± 11.2 years; ejection fraction 62.9 ± 6.0%; LA diameter 43.1 ± 4.9 mm; RA diameter 51.7 ± 8.3 × 42.9 ± 3.7 mm), the AF cycle length in RAA (134.0 ± 10.9 ms) was the shortest, and the fastest frequency potentials were located in the RAA in 65% of patients. For the left atrium, the AF cycle length of the roof (145.5 ± 14.9 ms) was the shortest, followed by the left atrial appendage (153.7 ± 17.1 ms) and bottom (154.8 ± 11.8 ms). High-frequency potentials of RAA could be rapidly conducted to left atrium via sagittal bundle and Bachmann's bundle, and the conduction time (55.0 ± 5.0 ms) was significantly shorter than the mean bi-atrial activation time (176.7 ± 10.3 ms, P < 0.0001). AF could be terminated after ablation at the RAA base (17 patients) or mechanical stimulation within the RAA (3 patients). To date, only two patients had recurrent atrial flutter, while the remaining patients maintained sinus rhythm. CONCLUSION: The AF driven by RAA is characterized by high-frequency potentials in RAA, and ablation at the RAA base can achieve a satisfactory therapeutic effect.

Role and mechanism of lncRNA under magnetic nanoparticles in atrial autonomic nerve remodeling during radiofrequency ablation of recurrent atrial fibrillation.

It aimed to investigate the mechanism of magnetic nanoparticles (MNPs) on atrial fibrillation and effect of n-isopropyl acrylamide coated MNPs (NIPA-co-MN) on the treatment of atrial fibrillation. Ten beagles weighing 20 - 25 kg were randomly divided into test group and control group. Dogs with atrial fibrillation were set as test group, and non-atrial fibrillation dogs as control group. The expression of long non-coding RNA (lncRNA) differentially expressed in the right anterior adipose pad in atrial fibrillation and non-atrial fibrillation dogs was detected by high-throughput sequencing. The relationship between lncRNA and cardiac autonomic nerve remodeling (CANR) was explored. In addition, 20 beagles weighing 20-25 kg were selected to study the therapeutic effect of n-isopropylacrylamide magnetic nanoparticles (NIPA-co-MN) on atrial fibrillation, and statistical analysis was performed. The volume and number of new neurons in the anterior right fat pad of atrium of test group were larger than the control group. The test group dogs produced 45 brand-new lncRNA, including 15 up-regulated transcripts and 30 down-regulated transcripts. MNPs injection can slow down the reduction of ventricular rate in right inferior ganglion plexus. The anterior right ganglion plexus resulted in a reduced amplitude of sinus tachyarrhythmia. This study provided references for the discovery of new diagnostic biomarkers or therapeutic targets and for the treatment of patients with atrial fibrillation.

Study on the role and mechanism of lncRNA in the remodeling of atrial energy metabolism in rabbits with atrial fibrillation based on nano sensor technology.

The purpose is to reveal the role and mechanism of long non-coding ribonucleic acid (lncRNA) in atrial fibrillation (AF) and atrial energy metabolism remodeling. The healthy adult New Zealand rabbit was chosen as the experimental animal, and the AF rabbit models were built. Besides, the lncRNA sequencing method based on nano sensor technology was employed to detect the differentially expressed lncRNAs, and the target lncRNA and its target genes were determined through bioinformatics analysis. Subsequently, TCONS_00016478 dysfunction experiment was performed. The gene level and protein level of TCONS_00016478, peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-α), and its downstream genes were detected. The results show that after sequencing, 99,755 new lncRNAs transcripts are found in total, of which 1,215 are significantly differentially expressed, 974 are down-regulated, and 241 are up-regulated. A new transcript TCONS_00016478 associated with the remodeling of atrial energy metabolism is further screened. Silencing TCONS_00016478 can significantly reduce PGC1-α, PPARγ, GLUT4, and CPT1 expression levels (P < 0.05). Thereby, TCONS_00016478 can affect the atrial energy metabolism remodeling and atrial fibrillation in experimental rabbits by regulating the PGC1-α/PPARγ signaling pathway.

Meta-analysis of high power short duration in atrial fibrillation ablation - a superior efficient ablation strategy.

BACKGROUND: The high power short duration (HPSD) approach was hoped to further improve the efficacy and safety in radiofrequency ablation of atrial fibrillation (AF), compared with Low power long duration (LPLD). However, the conclusion was controversial based on the previous limited data. The aim of this meta-analysis was to evaluate whether the clinical benefits of HPSD are superior to that of LPLD. METHODS: The PubMed, OVID, the Cochrane Library, and Elsevier's ScienceDirect databases were searched for clinical studies to compare HPSD and LPLD approach by simple search strings benefiting to a wider screened scope. RESULTS: Fifteen trials with 3255 patients were included in this analysis. Pooled analyses suggested that HPSD was associated with a lower recurrence of atrial tachyarrhythmias (ATAs) at 1-year follow-up (OR: 0.49; 95% CI: 0.35 to 0.67, p < .0001), benefitted from AF recurrence reduced (OR: 0.46; 95% CI: 0.31 to 0.67, p < .0001), rather than atrial tachycardia/atrial flutter (AT/AFL), but similar at 6 months follow-up, with a decreased oesophageal thermal injury (ETI) (OR: 0.48; 95% CI: 0.30 to 0.77, p = .002). Meanwhile, the HPSD approach benefitted to increase first-pass pulmonary vein isolation (FPI) (OR: 0.47; 95% CI: 0.34 to 0.64, p < .00001) and decrease acute pulmonary vein re-isolation (PVR) (OR: 0.45; 95% CI: 0.35 to 0.58, p < .00001), both mainly embodied in left pulmonary veins (PVs). HPSD showed a decreased procedural time (SMD: -0.95; 95% CI: -1.06 to -0.85, p < .00001), ablation number for pulmonary vein isolation (PVI) (SMD: -0.41; 95% CI: -0.58 to -0.24, p < .00001) and fluoroscopy time (SMD: -0.22; 95% CI: -0.32 to -0.12, p < .0001), which benefits from PVI + additional ablation strategy (SMD: -0.33; 95% CI: -0.46 to -0.21, p < .0001). CONCLUSIONS: The HPSD approach was associated with decreasing post-ablation AF recurrence in the 1-year follow-up, ETI, acute PVR (increasing FPI correspondingly), procedural time, ablation number for PVI and fluoroscopy time, benefitted to improve clinical outcomes and procedural process with improved safety.

CTRP13 Protects H9c2 Cells Against Hypoxia/Reoxygenation (H/R)-Induced Injury Via Regulating the AMPK/Nrf2/ARE Signaling Pathway.

Myocardial infarction (MI) is identified as the myocardial necrosis due to myocardial ischemia/reperfusion (I/R) injury and remains a leading cause of mortality. C1q/TNF-related protein 13 (CTRP13) is a member of CTRP family that has been found to be involved in coronary artery disease (CAD). However, the role of CTRP13 in MI remains unclear. We aimed to explore the functional role of CTRP13 in H9c2 cells exposed to hypoxia/reoxygenation (H/R). Our results demonstrated that H/R stimulation significantly decreased the expression of CTRP13 in H9c2 cells. H/R-induced an increase in ROS production and reductions in activities of SOD and CAT were prevented by CTRP13 overexpression but were aggravated by CTRP13 silencing. Moreover, CTRP13 overexpression could reverse the inductive effect of H/R on caspase-3 activity and bax expression, as well as the inhibitory effect of H/R on bcl-2 expression in H9c2 cells. However, CTRP13 silencing presented opposite effects with CTRP13 overexpression. Furthermore, CTRP13 overexpression enhanced the H/R-stimulated the expression levels of p-AMPK and nuclear Nrf2, and Nrf2 transcriptional activity. However, inhibition of AMPK reversed the CTRP13-mediated activation of Nrf2/ARE signaling and the cardiac-protective effect in H/R-exposed H9c2 cells. Additionally, silencing of Nrf2 reversed the protective effects of CTRP13 against H/R-stimulated oxidative stress and apoptosis in H9c2 cells. Finally, recombinant CTRP13 protein attenuated myocardial I/R-induced injury in rats. Taken together, these findings indicated that CTRP13 protected H9c2 cells from H/R-stimulated oxidative stress and apoptosis via regulating the AMPK/Nrf2/ARE signaling pathway. Our results provided evidence for the therapeutic potential of CTRP13 in myocardial I/R injury.