Irisin ameliorates UUO-induced renal interstitial fibrosis through TGF-ß1/periostin/MMP-2 signaling pathway.

Renal fibrosis is the most common pathway in progressive kidney diseases. The unilateral ureteral obstruction (UUO) model is used to induce progressive renal fibrosis. We evaluated the effects of irisin on renal interstitial fibrosis in UUO mice. The GSE121190, GSE36496, GSE42303, and GSE96101 datasets were downloaded from the Gene Expression Omnibus (GEO) database. In total, 656 differentially expressed genes (DEGs) were identified in normal and UUO mouse renal samples. Periostin and matrix metalloproteinase-2 (MMP-2) were selected to evaluate the effect of irisin on renal fibrosis in UUO mice. In UUO mice, irisin ameliorated renal function, decreased the expression of periostin and MMP-2, and attenuated epithelial-mesenchymal transition and extracellular matrix deposition in renal tissues. In HK-2 cells, irisin treatment markedly attenuated TGF-ß1-induced expression of periostin and MMP-2. Irisin treatment also inhibited TGF-ß1-induced epithelial-mesenchymal transition, extracellular matrix formation, and inflammatory responses. These protective effects of irisin were abolished by the overexpression of periostin and MMP-2. In summary, irisin treatment can improve UUO-induced renal interstitial fibrosis through the TGF-ß1/periostin/MMP-2 signaling pathway, suggesting that irisin may be used for the treatment of renal interstitial fibrosis.

Circulating mitochondria promoted endothelial cGAS-derived neuroinflammation in subfornical organ to aggravate sympathetic overdrive in heart failure mice.

BACKGROUND: Sympathoexcitation contributes to myocardial remodeling in heart failure (HF). Increased circulating pro-inflammatory mediators directly act on the Subfornical organ (SFO), the cardiovascular autonomic center, to increase sympathetic outflow. Circulating mitochondria (C-Mito) are the novel discovered mediators for inter-organ communication. Cyclic GMP-AMP synthase (cGAS) is the pro-inflammatory sensor of damaged mitochondria. OBJECTIVES: This study aimed to assess the sympathoexcitation effect of C-Mito in HF mice via promoting endothelial cGAS-derived neuroinflammation in the SFO. METHODS: C-Mito were isolated from HF mice established by isoprenaline (0.0125 mg/kg) infusion via osmotic mini-pumps for 2 weeks. Structural and functional analyses of C-Mito were conducted. Pre-stained C-Mito were intravenously injected every day for 2 weeks. Specific cGAS knockdown (cGAS KD) in the SFO endothelial cells (ECs) was achieved via the administration of AAV9-TIE-shRNA (cGAS) into the SFO. The activation of cGAS in the SFO ECs was assessed. The expression of the mitochondrial redox regulator Dihydroorotate dehydrogenase (DHODH) and its interaction with cGAS were also explored. Neuroinflammation and neuronal activation in the SFO were evaluated. Sympathetic activity, myocardial remodeling, and cardiac systolic dysfunction were measured. RESULTS: C-Mito were successfully isolated, which showed typical structural characteristics of mitochondria with double-membrane and inner crista. Further analysis showed impaired respiratory complexes activities of C-Mito from HF mice (C-MitoHF) accompanied by oxidative damage. C-Mito entered ECs, instead of glial cells and neurons in the SFO of HF mice. C-MitoHF increased the level of ROS and cytosolic free double-strand DNA (dsDNA), and activated cGAS in cultured brain endothelial cells. Furthermore, C-MitoHF highly expressed DHODH, which interacted with cGAS to facilitate endothelial cGAS activation. C-MitoHF aggravated endothelial inflammation, microglial/astroglial activation, and neuronal sensitization in the SFO of HF mice, which could be ameliorated by cGAS KD in the ECs of the SFO. Further analysis showed C-MitoHF failed to exacerbate sympathoexcitation and myocardial sympathetic hyperinnervation in cGAS KD HF mice. C-MitoHF promoted myocardial fibrosis and hypertrophy, and cardiac systolic dysfunction in HF mice, which could be ameliorated by cGAS KD. CONCLUSION: Collectively, we demonstrated that damaged C-MitoHF highly expressed DHODH, which promoted endothelial cGAS activation in the SFO, hence aggravating the sympathoexcitation and myocardial injury in HF mice, suggesting that C-Mito might be the novel therapeutic target for sympathoexcitation in HF.

Integrative Proteomic Analysis Reveals the Cytoskeleton Regulation and Mitophagy Difference Between Ischemic Cardiomyopathy and Dilated Cardiomyopathy.

Ischemic cardiomyopathy (ICM) and dilated cardiomyopathy (DCM) are the two primary etiologies of end-stage heart failure. However, there remains a dearth of comprehensive understanding the global perspective and the dynamics of the proteome and phosphoproteome in ICM and DCM, which hinders the profound comprehension of pivotal biological characteristics as well as differences in signal transduction activation mechanisms between these two major types of heart failure. We conducted high-throughput quantification proteomics and phosphoproteomics analysis of clinical heart tissues with ICM or DCM, which provided us the system-wide molecular insights into pathogenesis of clinical heart failure in both ICM and DCM. Both protein and phosphorylation expression levels exhibit distinct separation between heart failure and normal control heart tissues, highlighting the prominent characteristics of ICM and DCM. By integrating with omics results, Western blots, phosphosite-specific mutation, chemical intervention, and immunofluorescence validation, we found a significant activation of the PRKACA-GSK3ß signaling pathway in ICM. This signaling pathway influenced remolding of the microtubule network and regulated the critical actin filaments in cardiac construction. Additionally, DCM exhibited significantly elevated mitochondria energy supply injury compared to ICM, which induced the ROCK1-vimentin signaling pathway activation and promoted mitophagy. Our study not only delineated the major distinguishing features between ICM and DCM but also revealed the crucial discrepancy in the mechanisms between ICM and DCM. This study facilitates a more profound comprehension of pathophysiologic heterogeneity between ICM and DCM and provides a novel perspective to assist in the discovery of potential therapeutic targets for different types of heart failure.

Global research trends in unilateral ureteral obstruction-induced renal fibrosis: A bibliometric and visualized study.

BACKGROUND: Renal fibrosis is considered the pathway from almost all chronic kidney diseases (CKD) to end-stage renal diseases. The unilateral ureteral obstruction (UUO) model is a well-established experimental animal model to simulate renal fibrosis associated with obstructive nephropathy in an accelerated manner. In this study, in order to understand the development trends of research on UUO-induced renal fibrosis between 2005 and 2022 and predict prospects, we conducted a comprehensive bibliometric and visualized study using Web of Science (WoS). METHODS: The articles regarding UUO-induced renal fibrosis were culled from the "Core Collection" of the WoS database. VOSviewer software and the R-Bibliometrix Package were used in visual analysis of countries/regions, journals, authors, keywords, institutions, and highly cited articles in this field. RESULTS: The number of articles regarding UUO-induced renal fibrosis has obviously increased annually. China had the largest number of publications in this field. The most frequently used keywords were "inflammation," "transforming growth factor-beta1," "oxigative stress," "smad3," "beta-catenin," and "autophagy." Am J Physiol-Renal was the leading journal. The most highly influential documents were published by Higgins DF and his colleagues, with 46 local citations and 749 global citations. The leading institution was Nanjing Medical University. Furthermore, Zhang Y. was the author who contributed most to this field. CONCLUSION: Our results suggest that the molecular mechanism of UUO-induced renal fibrosis remains a research hot topic, especially on the inflammatory response and oxidative stress, and international cooperation is expected to expand and deepen in the future.

High-Performance MoS2/SWCNT Composite Films for a Flexible Thermoelectric Power Generator.

Single-walled carbon nanotube (SWCNT)-based thermoelectric materials have been extensively studied in the field of flexible wearable devices due to their high flexibility and excellent electrical conductivity (σ). However, poor Seebeck coefficient (S) and high thermal conductivity limit their thermoelectric application. In this work, free-standing MoS2/SWCNT composite films with improved thermoelectric performance were fabricated by doping SWCNTs with MoS2 nanosheets. The results demonstrated that the energy filtering effect at the MoS2/SWCNT interface increased the S of composites. In addition, the σ of composites was also improved due to the reason that S-π interaction between MoS2 and SWCNTs made good contact between MoS2 and SWCNTs and improved carrier transport. Finally, the obtained MoS2/SWCNT showed a maximum power factor of 131.9 ± 4.5 µW m-1 K-2 at room temperature with a σ of 680 ± 6.7 S cm-1 and an S of 44.0 ± 1.7 µV K-1 at a MoS2/SWCNT mass ratio of 15:100. As a demonstration, a thermoelectric device composed of three pairs of p-n junctions was prepared, which exhibited a maximum output power of 0.43 µW at a temperature gradient of 50 K. Therefore, this work offers a simple method of enhancing the thermoelectric properties of SWCNT-based materials.

Cardiac-specific BACH1 ablation attenuates pathological cardiac hypertrophy by inhibiting the Ang II type 1 receptor expression and the Ca2+/CaMKII pathway.

AIMS: BACH1 is up-regulated in hypertrophic hearts, but its function in cardiac hypertrophy remains largely unknown. This research investigates the function and mechanisms of BACH1 in the regulation of cardiac hypertrophy. METHODS AND RESULTS: Male cardiac-specific BACH1 knockout mice or cardiac-specific BACH1 transgenic (BACH1-Tg) mice and their respective wild-type littermates developed cardiac hypertrophy induced by angiotensin II (Ang II) or transverse aortic constriction (TAC). Cardiac-specific BACH1 knockout in mice protected the hearts against Ang II- and TAC-induced cardiac hypertrophy and fibrosis, and preserved cardiac function. Conversely, cardiac-specific BACH1 overexpression markedly exaggerated cardiac hypertrophy and fibrosis and reduced cardiac function in mice with Ang II- and TAC-induced hypertrophy. Mechanistically, BACH1 silencing attenuated Ang II- and norepinephrine-stimulated calcium/calmodulin-dependent protein kinase II (CaMKII) signalling, the expression of hypertrophic genes, and hypertrophic growth of cardiomyocytes. Ang II stimulation promoted the nuclear localization of BACH1, facilitated the recruitment of BACH1 to the Ang II type 1 receptor (AT1R) gene promoter, and then increased the expression of AT1R. Inhibition of BACH1 attenuated Ang II-stimulated AT1R expression, cytosolic Ca2+ levels, and CaMKII activation in cardiomyocytes, whereas overexpression of BACH1 led to the opposite effects. The increased expression of hypertrophic genes induced by BACH1 overexpression upon Ang II stimulation was suppressed by CaMKII inhibitor KN93. The AT1R antagonist, losartan, significantly attenuated BACH1-mediated CaMKII activation and cardiomyocyte hypertrophy under Ang II stimulation in vitro. Similarly, Ang II-induced myocardial pathological hypertrophy, cardiac fibrosis, and dysfunction in BACH1-Tg mice were blunted by treatment with losartan. CONCLUSION: This study elucidates a novel important role of BACH1 in pathological cardiac hypertrophy by regulating the AT1R expression and the Ca2+/CaMKII pathway, and highlights potential therapeutic target in pathological cardiac hypertrophy.

Irisin Ameliorates Renal Tubulointerstitial Fibrosis by Regulating the Smad4/ß-Catenin Pathway in Diabetic Mice.

Background: The primary pathophysiology of diabetic kidney disease (DKD) is tubulointerstitial fibrosis (TIF), and an essential contributing element is excessive extracellular matrix deposition. Irisin is a polypeptide formed by splitting fibronectin type III domain containing 5 (FNDC5), which participates in a number of physiological and pathological processes. Methods: The purpose of this article is to examine irisin's function in DKD and analyze both its in vitro and in vivo effects. The Gene Expression Omnibus (GEO) database was used to download GSE30122, GSE104954, and GSE99325. Analysis of renal tubule samples from nondiabetic and diabetic mice identified 94 differentially expressed genes (DEGs). The transforming growth factor beta receptor 2 (TGFBR2), irisin, and TGF-ß1 were utilized as DEGs to examine the impact of irisin on TIF in diabetic kidney tissue, according to the datasets retrieved from the GEO database and Nephroseq database. Additionally, the therapeutic impact of irisin was also examined using Western blot, RT-qPCR, immunofluorescence, immunohistochemistry, and kits for detecting mouse biochemical indices. Results: In vitro, the findings demonstrated that irisin not only down-regulated the expression of Smad4 and ß-catenin but also reduced the expression of proteins linked to fibrosis, the epithelial-mesenchymal transition (EMT), and mitochondrial dysfunction in HK-2 cells maintained in high glucose (HG) environment. In vivo, overexpressed FNDC5 plasmid was injected into diabetic mice to enhance its expression. Our studies found that overexpressed FNDC5 plasmid not only reversed the biochemical parameters and renal morphological characteristics of diabetic mice but also alleviated EMT and TIF by inhibiting Smad4/ß-catenin signaling pathway. Conclusion: The above experimental results revealed that irisin could reduce TIF in diabetic mice via regulating the Smad4/ß-catenin pathway.

Single-pixel imaging with high spectral and spatial resolution.

It has long been a challenge to obtain high spectral and spatial resolution simultaneously for the field of measurement and detection. Here we present a measurement system based on single-pixel imaging with compressive sensing that can realize excellent spectral and spatial resolution at the same time, as well as data compression. Our method can achieve high spectral and spatial resolution, which is different from the mutually restrictive relationship between the two in traditional imaging. In our experiments, 301 spectral channels are obtained in the band of 420-780 nm with a spectral resolution of 1.2 nm and a spatial resolution of 1.11 mrad. A sampling rate of 12.5% for a 64×64p i x e l image is obtained by using compressive sensing, which also reduces the measurement time; thus, high spectral and spatial resolution are realized simultaneously, even at a low sampling rate.

Sestrin2 remedies podocyte injury via orchestrating TSP-1/TGF-ß1/Smad3 axis in diabetic kidney disease.

Sestrin2 is identified as a stress-induced protein and could functionate in many aspects. In our study, we investigated the latent impact of Sestrin2 on podocyte injury and its molecular mechanism in vivo and in vitro in diabetic kidney disease (DKD). Sestrin2 was low-expressed in renal biopsies from individuals with DKD, the glomeruli from diabetic mice, and mouse podocytes exposed to high glucose (HG). Sestrin2 overexpression ameliorated HG-induced phenotypic alterations, apoptosis, and oxidative stress in conditionally immortalized mouse podocytes and modulated the activity of Thrombospondin-1 (TSP-1)/transforming growth factor (TGF-ß1)/Smad3 pathway in podocytes. Moreover, TSP-1 inhibitor LSKL or TGF-ß blocker Pirfenidone arrested podocyte injury induced by HG. Streptozotocin (STZ) was employed to render equivalent diabetes in B6-TgN (CMV-Sestrin2) (TgN) and wild-type (WT) control mice. Sestrin2 alleviated increased levels of 24-h urinary protein, blood urea nitrogen, serum creatinine and triglyceride, and urine 8-OHdG in diabetic mice. Podocyte phenotypic alterations, increased expression of apoptosis-associated proteins and podocyte loss were observed in WT but not in diabetic TgN mice, as well as oxidative stress. Additionally, TSP-1/TGF-ß1/Smad3 signaling pathway was also suppressed in glomeruli of diabetic TgN mice. Thus, Sestrin2 mitigates podocyte injury in DKD via orchestrating TSP-1/TGF-ß1/Smad3 pathway, underlining Sestrin2 as a promising therapeutic target for DKD.

Mini-Invasive Bentall Procedure Performed via a Right Anterior Thoracotomy Approach With a Costochondral Cartilage Sparing.

Objectives: A right minithoracotomy approach with a sternal sparing technique is a minimally invasive option for surgeons performing aortic root surgery. This report presents our initial clinical results of the right minithoracotomy Bentall procedure. Methods: Clinical data of 15 patients were retrospectively analyzed who underwent the minimally invasive Bentall procedure through the right anterior thoracotomy via the second intercostal incision without any costochondral cartilage invasion at our institution between October, 2019 and June, 2021. The operative time, length of intensive care unit stay and postoperative hospital stay, perioperative outcomes, and follow-up results were analyzed. Results: The median aortic cross-clamping time was 95.0 (85.5-98.8) min. Three (21.4%) patients received blood transfusion. The median drainage volume in the first 24 h was 200.0 ml, with no redo for bleeding. The median duration of mechanical ventilation was 12.5 (11.0-25.0) h, and median length of intensive care unit stay was 1.5 (1.0-3.0) day. All patients discharged 5.8 ± 1.2 days following surgery, with no dead patients found. At 6 months following surgery, all patients survived with an improved New York Heart Association (NYHA) functional class. Conclusion: The right minithoracotomy Bentall procedure may be performed safely with low morbidity and mortality. This approach should be considered as an option in carefully selected patients requiring aortic root replacement.

Image-free real-time target tracking by single-pixel detection.

Image-based target tracking methods rely on continuous image acquisition and post-processing, which will result in low tracking efficiency. To realize real-time tracking of fast moving objects, we propose an image-free target tracking scheme based on the discrete cosine transform and single-pixel detection. Our method avoids calculating all the phase values, so the number of samples can be greatly reduced. Furthermore, complementary modulation is applied to reduce the measurement noise, and background subtraction is applied to enhance the contrast. The results of simulations and experiments demonstrate that the proposed scheme can accomplish the tracking task in a complex background with a sampling ratio of less than 0.59% of the Nyquist-Shannon criterion, thereby significantly reducing the measurement time. The tracking speed can reach 208 fps at a spatial resolution of 128 × 128 pixels with a tracking error of no more than one pixel. This technique provides a new idea for real-time tracking of fast-moving targets.

PP2 Ameliorates Renal Fibrosis by Regulating the NF-κB/COX-2 and PPARγ/UCP2 Pathway in Diabetic Mice.

Renal fibrosis is characterized by glomerulosclerosis and tubulointerstitial fibrosis in diabetic nephropathy (DN). We aimed to evaluate the effects of PP2 on renal fibrosis of DN. GSE33744 and GSE86300 were downloaded from the GEO database. Firstly, 839 DEGs were identified between nondiabetic and diabetic mice renal glomerular samples. COX-2 was selected to assess the effects of PP2 on renal glomerulosclerosis. In db/db mice, PP2 decreased the expression of COX-2, phosphorylated p65, and fibrotic proteins, accompanied with attenuated renal glomerulosclerosis. In cultured glomerular mesangial cells, high glucose- (HG-) induced p65 phosphorylation and COX-2 expression were attenuated by PP2 or NF-κB inhibitor PDTC. PP2, PDTC, or COX-2 inhibitor NS-398 ameliorated abnormal proliferation and expression of fibrotic proteins induced by HG. Secondly, 238 DEGs were identified between nondiabetic and diabetic mice renal cortex samples. UCP2 was selected to assess the effects of PP2 on renal tubulointerstitial fibrosis. In db/db mice, PP2 decreased the expression of PPARγ and UCP2, accompanied with attenuated renal tubulointerstitial fibrosis and EMT. In cultured proximal tubular cells, HG-induced PPARγ and UCP2 expression was inhibited by PP2 or PPARγ antagonist GW9662. PP2, GW9662, or UCP2 shRNA ameliorated HG-induced EMT. These results indicated that PP2 ameliorated renal fibrosis in diabetic mice.

Enlargement of left ventricular outflow tract using an autologous pericardial patch for anterior mitral valve leaflet and septal myectomy through trans-mitral approach for the treatment of hypertrophic obstructive cardiomyopathy.

OBJECTIVE: Modified Morrow procedure is the gold standard of surgical intervention for hypertrophic obstructive cardiomyopathy (HOCM). However, there are certain cases without complete relief of obstruction through trans-aortic approach, we, therefore, described an unusual technique. We aimed to retrospectively analyze this series of patients to reveal its safety and efficiency. METHODS: We retrospectively analyzed a total of 247 consecutive HOCM patients in our center from January 2016 to December 2019. Sixteen of them who underwent enlargement of left ventricular outflow tract (LVOT) using an autologous pericardial patch for anterior mitral valve leaflet and septal myectomy through trans-mitral approach were recruited in this study. Baseline characteristics, perioperative data, and the outcomes were studied. RESULTS: Of the 16 patients, there was no operative mortality. No permanent pacemaker implantation and ventricular septal defects formation were observed. The peak pressure gradient of LVOT decreased from 97.56 ± 23.81 mmHg to 7.56 ± 2.13 mmHg (p < .01) after operation and 10.19 ± 2.93 mmHg (p < .01) 3 months later. The average septal thickness decreased from 18.38 ± 3.56 mm to 10.00 ± 2.74 mm (p < .01). During a mean follow-up of 34.25 ± 12.85 months (range, 15-57), no patient required cardiac reoperation. At the last follow up, the mean peak pressure gradient of LVOT was 10.12 ± 2.03 mmHg and no patient had more than moderate mitral regurgitation. CONCLUSION: Enlargement of LVOT using an autologous pericardial patch for anterior mitral valve leaflet and septal myectomy through trans-mitral approach is feasible and reliable for the treatment of certain types of HOCM cases.

Development and validation of a nomogram to better predict hypertension based on a 10-year retrospective cohort study in China.

Background: Hypertension is a highly prevalent disorder. A nomogram to estimate the risk of hypertension in Chinese individuals is not available. Methods: 6201 subjects were enrolled in the study and randomly divided into training set and validation set at a ratio of 2:1. The LASSO regression technique was used to select the optimal predictive features, and multivariate logistic regression to construct the nomograms. The performance of the nomograms was assessed and validated by AUC, C-index, calibration curves, DCA, clinical impact curves, NRI, and IDI. Results: The nomogram140/90 was developed with the parameters of family history of hypertension, age, SBP, DBP, BMI, MCHC, MPV, TBIL, and TG. AUCs of nomogram140/90 were 0.750 in the training set and 0.772 in the validation set. C-index of nomogram140/90 were 0.750 in the training set and 0.772 in the validation set. The nomogram130/80 was developed with the parameters of family history of hypertension, age, SBP, DBP, RDWSD, and TBIL. AUCs of nomogram130/80 were 0.705 in the training set and 0.697 in the validation set. C-index of nomogram130/80 were 0.705 in the training set and 0.697 in the validation set. Both nomograms demonstrated favorable clinical consistency. NRI and IDI showed that the nomogram140/90 exhibited superior performance than the nomogram130/80. Therefore, the web-based calculator of nomogram140/90 was built online. Conclusions: We have constructed a nomogram that can be effectively used in the preliminary and in-depth risk prediction of hypertension in a Chinese population based on a 10-year retrospective cohort study. Funding: This study was supported by the Hebei Science and Technology Department Program (no. H2018206110).

A New Method for Analyzing Aero-Optical Effects with Transient Simulation.

Aero-optical effects reduce the accuracy of optical sensors on high-speed aircraft. Current research usually focuses on light refraction caused by large-scale density structures in turbulence. A method for analyzing photon energy scattering caused by micro-scale structures is proposed in this paper, which can explain the macro image distortion caused by moving molecules in inhomogeneous airflow. Quantitative analysis of the propagation equation indicates that micro-scale structures may contribute more to the wavefront distortion than the widely considered large-scale structures. To analyze the micro mechanism of aero-optical effects, a transient simulator is designed based on the scaling model of transient distorted wavefronts and the artificial vortex structure. The simulation results demonstrate that correct aero-optical phenomena can be obtained from the micro mechanism of photon energy scattering. Examples of using the transient simulator to optimize the parameters of the star sensor on a hypersonic vehicle are provided. The proposed analysis method for micro-scale structures provides a new idea for studying the aero-optical effects.

Unusual cardiac tamponade: Giant primary cardiac myxoid liposarcoma.

Primary cardiac myxoid liposarcoma is an extremely rare disease. We reported a 61-year-old man with a 1-month history of aggressive dyspnea and anorexia due to a giant primary cardiac myxoid liposarcoma. Radical resection, whenever feasible, is considered to be an appropriate surgical strategy for this disease. Heart transplantation may be an alternative therapy for such isolated and unresectable tumor.

Giant cardiac myxoma presenting with exertional angina: Coronary steal due to neovascularization?

Myxoma is the most common benign tumor of the heart. Most patients present with no symptoms, only a few patients present with exertional dyspnea and stroke. We introduce this rare case presenting with exertional angina, which was caused by coronary steal due to neovascularization, proved by coronary angiography and cardiac stress testing.

Mitral valve repair and surgical ablation for atrial functional mitral regurgitation.

BACKGROUND: This observational study aimed to share our experience in the surgical management of atrial functional mitral regurgitation (AFMR). METHODS: We retrospectively identified 82 AFMR patients (63.6±7.7 years) from June 2008 to November 2018 at our institution. Of these patients, 72.0% of them were classified as NYHA functional class III/IV, and all of them had persistent AF. All patients underwent mitral valve (MV) repair, and 52 (63.4%) received concomitant surgical ablation (SA). Patients were followed up for 26.1±27.6 months, and postoperative mitral regurgitation (MR) was assessed by echocardiography. RESULTS: There was no in-hospital mortality. The overall 1-year and 3-year survival rates were 97.5% and 92.9%, respectively, and 96.1% of patients recovered to NYHA functional class I/II at the latest follow-up. The left atrium (LA) diameter (P<0.001), left ventricular (LV) end-diastolic diameter (P<0.001), LV end-systolic diameter (LVESD) (P<0.001) and pulmonary artery pressure (P=0.006) significantly decreased postoperatively. The overall 1-year and 3-year freedom from recurrent MR rates were 94.3% and 65.3%, respectively, and a significant difference was found between the SA group and the non-SA group (93.8% and 93.8% vs. 95.5% and 44.2%, P=0.035). In a subgroup analysis, this significant difference was only found in the small LA group (≤60 mm). CONCLUSIONS: Our results suggest that MV repair for AFMR is safe and effective. It improves heart failure symptoms and results in reverse-remodeling of both the LA and LV. Concomitant SA might benefit patients in terms of recurrent MR, especially in the small LA group (≤60 mm).