Midterm Outcome of Valve Repair for Rheumatic Mitral Stenosis: 6-year Experience in a Single Mid-Volume Cardiac Center.

OBJECTIVES: Previous studies have reported satisfactory long-term results of mitral valve (MV) repair for rheumatic mitral disease. However, the effects of this procedure in isolated rheumatic mitral stenosis remain unclear. In addition, protective effects of MV repair on cardiac function have not been verified in rheumatic MV disease. This study retrospectively evaluated early mortality and mid-term results of MV repair for isolated rheumatic mitral stenosis in a mid-volume cardiac centre, and explored the effects of this procedure on cardiac function. METHODS: Between January 2015 and May 2021, 360 patients with isolated rheumatic mitral stenosis and combined (concomitant) atrial fibrillation (AF) underwent MV repair (100 patients) or MV replacement (260 patients). Perioperative characteristics were compared between the two groups and a regression analysis for early mortality and mid-term left ventricular ejection fraction was conducted. In addition, mid-term survival was compared between the two groups. RESULTS: Baseline characteristics of the two groups were balanced after matching. Compared with patients in the replacement group, patients with MV repair had a lower occurrence of postoperative hypotension and AF. There was no difference in early mortality or mid-term survival between the two groups. However, MV repair was associated with a higher mid-term left ventricular ejection fraction. During follow-up, four thromboembolic events and four haemorrhagic events occurred in the replacement group. No blood coagulation-related complications occurred in the repair group. CONCLUSION: Mitral valve repair for isolated rheumatic mitral stenosis and concomitant AF was feasible in a mid-volume cardiac centre, with satisfactory perioperative results and mid-term outcomes. Furthermore, this procedure preserved mid-term left ventricular systolic function.

Outcome for concomitant mitral regurgitation after surgery for aortic insufficiency.

BACKGROUND: Moderate/severe aortic regurgitation (AR) with concomitant mitral regurgitation (MR) is a common multiple valve disease for which treatment strategies are controversial. The current study explored long-term outcomes of concomitant MR after AR surgery and the effect of combined mitral valvuloplasty. METHODS: A total of 506 patients with moderate/severe AR and concomitant MR undergoing aortic valve surgery between January 2013 and December 2021 in our cardiac center were enrolled. Risk factors for early mortality, late mortality and persistent MR were identified by logistic regression and generalized linear mixed model. RESULTS: At least one follow-up record was available for 96.3% patients up to May 2022 and 264 (66.8%) patients had no or trivial MR, 112 (28.4%) had mild MR, 16 (4.1%) had moderate MR and 3 (0.8%) patients had severe MR. Persistent MR was recorded for 92 (23.3%) patients during follow-up. Combined mitral valvuloplasty (odds ratio: 0.23; 95% confidential interval: 0.08-0.64; p = 0.005) and better left ventricular reverse remodeling (odds ratio: 0.99; 95% confidential interval: 0.986-0.996); p < 0.001) were found likely to reduce the possibility of persistent MR during follow-up. CONCLUSIONS: Most patients with moderate/severe AR and concomitant MR had a good long-term post-surgical outcome for MR. However, a few had persistent MR during follow-up. Combined mitral valvuloplasty and better left ventricular reverse remodeling reduced the possibility of long-term persistent MR.

Artificial Graft Replacement for the Pulmonary Artery Aneurysm: Three Case Reports.

Pulmonary artery aneurysm (PAA) is a relatively rare disease. The symptoms are usually nonspecific and often identified due to coughing or dyspnea. Pericardial tamponade caused by the PAA dissection or rupture is the most common cause of death, so active surgical treatment is recommended. The surgical reports in the literature are handful. Here we report three cases, all of whom were admitted due to exertional dyspnea. PAAs were observed from the main to the left and/or the right pulmonary artery. All three cases received PAA resection and artificial graft replacement with good outcomes.

Intrinsic left ventricular impairment in Marfan syndrome: A systematic review and meta-analysis.

BACKGROUND: Intrinsic cardiac impairment in Marfan syndrome (MFS) has been explored in many clinical studies; however, their results have been inconsistent. This meta-analysis aimed to assess the difference in cardiac structure and function between Marfan patients and healthy individuals, and to verify the hypothesis of intrinsic cardiac impairment in MFS. METHODS: Electronic searches for studies were performed in the PubMed, Embase, and Cochrane Library databases. Nine studies with 490 patients with MFS and 478 controls were included in the analysis. Age and sex were strictly matched between Marfan patients and healthy controls in every study. RESULTS: There was no difference in the left ventricular end systolic diameter index (mean difference [MD]: 0.33; 95% confidence interval [CI]: (-0.24, 0.89); p = 0.26) and left ventricular end diastolic diameter index (MD: 0.18; 95% CI: [-0.47, 0.83]; p = 0.58) between Marfan patients and controls. Marfan patients showed larger left ventricular end systolic volume index (MD: 2.62; 95% CI: [0.27, 4.97]; p = 0.03) and left ventricular end diastolic volume index (MD: 4.16; 95% CI: [2.70, 5.63]; p < 0.01) than the control group. Furthermore, Marfan patients showed a lower left ventricular ejection fraction than healthy people (MD: -2.59%; 95% CI: [-4.64%, -0.54%]; p = 0.01). CONCLUSIONS: Intrinsic cardiac impairment was observed in MFS. MFS patients showed the larger left ventricular volume and poorer left ventricular function than matched controls. Considering the potentially adverse impact on cardiac function, intrinsic cardiac impairment in MFS should be considered during the cardiac surgery.

Chitosan Hydrogel Enhances the Therapeutic Efficacy of Bone Marrow-Derived Mesenchymal Stem Cells for Myocardial Infarction by Alleviating Vascular Endothelial Cell Pyroptosis.

Myocardial infarction (MI) is one of the higher mortality rates, and current treatment can only delay the progression of the disease. Experiments have shown that cell therapy could improve cardiac function and mesenchymal stem cells (MSCs)-based therapies provide a great promising approach in the treatment of MI. However, low cell survival and engraftment restricts the successful application of MSCs for treating MI. Here, we explored whether co-transplantation of a chitosan (CS) thermosensitive hydrogel with bone marrow-derived MSCs (BMSCs) could optimize and maximize the therapeutic of BMSCs in a mouse model of MI. The fate of transplanted BMSCs was monitored by bioluminescence imaging, and the recovery of cardiac function was detected by echocardiogram. Our results proved that CS hydrogel enhanced the BMSCs' survival and the recovery of cardiac function by protecting the vascular endothelial cells. Further studies revealed that the increased number of vascular endothelial cells was due to the fact that transplanted BMSCs inhibited the inflammatory response and alleviated the pyroptosis of vascular endothelial cells. In conclusions, CS hydrogel improved the engraftment of transplanted BMSCs, ameliorated inflammatory responses, and further promoted functional recovery of heart by alleviating vascular endothelial cell pyroptosis.

Cold-Adapted Glutathione S-Transferases from Antarctic Psychrophilic Bacterium Halomonas sp. ANT108: Heterologous Expression, Characterization, and Oxidative Resistance.

Glutathione S-transferases are one of the most important antioxidant enzymes to protect against oxidative damage induced by reactive oxygen species. In this study, a novel gst gene, designated as hsgst, was derived from Antarctic sea ice bacterium Halomonas sp. ANT108 and expressed in Escherichia coli (E. coli) BL21. The hsgst gene was 603 bp in length and encoded a protein of 200 amino acids. Compared with the mesophilic EcGST, homology modeling indicated HsGST had some structural characteristics of cold-adapted enzymes, such as higher frequency of glycine residues, lower frequency of proline and arginine residues, and reduced electrostatic interactions, which might be in relation to the high catalytic efficiency at low temperature. The recombinant HsGST (rHsGST) was purified to apparent homogeneity with Ni-affinity chromatography and its biochemical properties were investigated. The specific activity of the purified rHsGST was 254.20 nmol/min/mg. The optimum temperature and pH of enzyme were 25 °C and 7.5, respectively. Most importantly, rHsGST retained 41.67% of its maximal activity at 0 °C. 2.0 M NaCl and 0.2% H2O2 had no effect on the enzyme activity. Moreover, rHsGST exhibited its protective effects against oxidative stresses in E. coli cells. Due to its high catalytic efficiency and oxidative resistance at low temperature, rHsGST may be a potential candidate as antioxidant in low temperature health foods.

The Tumor Suppressive Role of MiRNA-509-5p by Targeting FOXM1 in Non-Small Cell Lung Cancer.

BACKGROUND/AIMS: Deregulation of microRNAs (miRNAs) expression is a frequent event in cancer development and progression. Recent studies have implied that abnormal expression of miRNAs is frequently observed in non-small cell lung cancer (NSCLC). Here, we examined the levels and biological functions of miR-509-5p in NSCLC. METHODS: The levels of miR-509-5p were measured by real-time quantitative PCR (RT-PCR) in NSCLC cell lines and NSCLC tissues along with adjacent normal tissues. Cell viability was analyzed by MTT and colony formation assay. Cell migration and invasion were evaluated by transwell and wound healing assay. In addition, we predicted the putative targets of miR-509-5p by bioinformatics analyses. Moreover, by luciferase-reporter assay, we analyzed the relationship between miR-509-5p and the target in NSCLC cells. RESULTS: miR-509-5p expression was significantly reduced in NSCLC tissues compared with adjacent normal tissues. In addition, miR-509-5p decreased cell proliferation, migration and invasive capability of NSCLC cells. Moreover, we found that FOXM1 was a putative target of miR-509-5p. Enforced miR-509-5p expression in NSCLC cells reduced both mRNA and protein levels of FOXM1. Furthermore, dual-luciferase reporter assay showed miR-509-5p could bind to the 3' untranslational regions of FOXM1 mRNA. Furthermore, overexpression of FOXM1 reversed cell viability, migration, invasion and vimentin levels suppressed by miR-509-5p mimics in H1299 cells. CONCLUSIONS: miR-509-5p exerts tumor-suppressive effects by attenuating FOXM1 in NSCLC. Collectively, these findings provide further evidence that miR-509-5p may be considered as a novel and potential target for the diagnosis, prognosis and treatment of NSCLC.

[Clinical analysis of tricuspid valve replacement].

OBJECTIVE: To summarize the outcome of tricuspid valve replacement.
 METHODS: A total of 28 patients (15 males and 13 females) underwent tricuspid valve replacement from March 2000 to February 2015 in the First Affiliated Hospital of Zhengzhou University were recruited. Among them, 16 patients were Ebstein's anomaly, 7 had rheumatic valve heart disease, 3 and 2 suffered from infective endocarditis and degenerative tricuspid lesions, respectively.
 RESULTS: One patient died of multiple organ failure. Four patients were implanted permanent cardiac pacemaker because of third degree atrioventricular block occurring in the 5th day (2 patients) and in the 9th day (2 patients) after the operation, respectively. Twenty-seven patients were followed up from 1 month to 15 years. The prosthetic valves and permanent pacemakers worked well.
 CONCLUSION: Third degree of atrioventricular block, mostly appearing in early postoperative period, is the most common and severe complication of tricuspid valve replacement. The key point for prevention of damage is to accurately identify the anatomical relationship among the tricuspid valve, atrioventricular node, and conduction bundle.

[Ventricular septal plication for post infarction anterior and anterior-septal aneurysm of the left ventricle].

OBJECTIVE: To determine the use of septal plication with Dor or Cooley procedure for post infarction anterior and anterior-septal aneurysm of the left ventricle. METHODS: A total of 23 patients with post infarction anterior and anterior-septal aneurysm of the left ventricle underwent septal plication and Dor or Cooley procedure along with coronary artery bypass grafting concomitantly. Data of NYHA grading, left ventricular end diastolic volume index (LVEDVI), left ventricular end systolic volume index (LVESVI) and left ventricular ejection fraction (LVEF) were recorded before the surgery, before discharge and 3 months after the surgery. RESULTS: Compared with the preoperative data, the NYHA grading before the discharge and 3 months after the surgery improved from 3.21 ± 0.62 to 1.72 ± 0.31 and 1.57 ± 0.23(P<0.05); LVEDVI decreased from (102.31 ± 18.71) mL/m² to (62.11 ± 6.21) mL/m² and (54.63 ± 4.54) mL/m² (P<0.05); LVESVI decreased from (69.32 ± 17.48) mL/m² to (30.23 ± 3.25)mL/m² and (28.34 ± 3.12) mL/m²; while LVEF increased from (32.92 ± 8.12)% to (48.78 ± 4.51)% and (50.52 ± 4.68)% (P<0.05), respectively. CONCLUSION: Ventricular septal plication combined with Dor or Cooley procedure can remarkably improve the left heart function in patients with post infarction ventricular aneurysm.

Genome-wide analysis revealed the dysregulation of RNA binding protein-correlated alternative splicing events in myocardial ischemia reperfusion injury.

BACKGROUND: Myocardial ischemia reperfusion injury (MIRI), the tissue damage which is caused by the returning of blood supply to tissue after a period of ischemia, greatly reduces the therapeutic effect of treatment of myocardial infarction. But the underlying functional mechanisms of MIRI are still unclear. METHODS: We constructed mouse models of MIRI, extracted injured and healthy myocardial tissues, and performed transcriptome sequencing experiments (RNA-seq) to systematically investigate the dysregulated transcriptome of MIRI, especially the alternative splicing (AS) regulation and RNA binding proteins (RBPs). Selected RBPs and MIRI-associated AS events were then validated by RT-qPCR experiments. RESULTS: The differentially expressed gene (DEG) analyses indicated that transcriptome profiles were changed by MIRI and that DEGs' enriched functions were consistent with MIRI's dysregulated pathways. Furthermore, the AS profile was synergistically regulated and showed clear differences between the mouse model and the healthy samples. The exon skipping events significantly increased in MIRI model samples, while the opposite cassette exon events significantly decreased. According to the functional analysis, regulated alternative splicing genes (RASGs) were enriched in protein transport, cell division /cell cycle, RNA splicing, and endocytosis pathways, which were associated with the development of MIRI. Meanwhile, 493 differentially expressed RBPs (DE RBPs) were detected, most of which were correlated with the changed ratios of AS events. In addition, nine DE RBP genes were validated, including Eif5, Pdia6, Tagln2, Vasp, Zfp36l2, Grsf1, Idh2, Ndrg2, and Uqcrc1. These nine DE RBPs were correlated with RASGs enriched in translation process, cell growth and division, and endocytosis pathways, highly consistent with the functions of all RASGs. Finally, we validated the AS ratio changes of five regulated alternative splicing events (RASEs) derived from important regulatory genes, including Mtmr3, Cdc42, Cd47, Fbln2, Vegfa, and Fhl2. CONCLUSION: Our study emphasized the critical roles of the dysregulated AS profiles in MIRI development, investigated the potential functions of MIRI-associated RASGs, and identified regulatory RBPs involved in AS regulation. We propose that the identified RASEs and RBPs could serve as important regulators and potential therapeutic targets in MIRI treatment in the future.

Anzhen Risk Evaluation System for Acute Aortic Syndrome (AZSCORE-AAS): protocol for a multicentre prospective cohort study in northern China.

INTRODUCTION: Acute aortic syndrome (AAS) is a group of acute and critical conditions, including acute aortic dissection (AAD), acute intramural haematoma and penetrating aortic ulcer. High mortality and morbidity rates result in a poor patient prognosis. Prompt diagnoses and timely interventions are paramount for saving patients' lives. In recent years, risk models for AAD have been established worldwide; however, a risk evaluation system for AAS is still lacking in China. Therefore, this study aims to develop an early warning and risk scoring system in combination with the novel potential biomarker soluble ST2 (sST2) for AAS. METHODS AND ANALYSIS: This multicentre, prospective, observational study will recruit patients diagnosed with AAS at three tertiary referral centres from 1 January 2020 to 31 December 2023. We will analyse the discrepancies in sST2 levels in patients with different AAS types and explore the accuracy of sST2 in distinguishing between them. We will also incorporate potential risk factors and sST2 into a logistic regression model to establish a logistic risk scoring system for predicting postoperative death and prolonged intensive care unit stay in patients with AAS. ETHICS AND DISSEMINATION: This study was registered on the Chinese Clinical Trial Registry website (http://www. chictr. org. cn/). Ethical approval was obtained from the human research ethics committees of Beijing Anzhen Hospital (KS2019016). The ethics review board of each participating hospital agreed to participate. The final risk prediction model will be published in an appropriate journal and disseminated as a mobile application for clinical use. Approval and anonymised data will be shared. TRIAL REGISTRATION NUMBER: ChiCTR1900027763.

SHP-1/STAT3 Interaction Is Related to Luteolin-Induced Myocardial Ischemia Protection.

Prevention and management of myocardial ischemia/reperfusion (I/R) injury is a key step in coronary heart disease surgery. Luteolin is a falconoid compound that has an antioxidant effect, but its mechanism in I/R injury in vivo and in vitro is still under explored. This study attempted to reveal the role of luteolin (Lut) in I/R through mediation of the Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP-1)/Signal transducer and activator of transcription 3 (STAT3) pathway. To establish I/R rat models, the left anterior descending artery (LAD) was ligated for 30 min and re-perfused for 1 h in Lut-pretreated or nude rats. Comparisons between infarct area, cardiac dysfunction, and myocardial cell death and inflammatory reaction were performed in I/R-induced rats. Hypoxia/reoxygenation (H/R) cell models were established by stimulating H9c2 cells with 95% nitrogen and 5% carbon dioxide. Simultaneously, H/R-related cell death and inflammatory reactions were investigated following Lut treatment. The target protein of Lut was identified using western blotting. Pro-inflammatory cytokines were also measured in serum or Lut-pretreated cell culture medium. The results revealed that compared with the I/R group, Lut treatment could significantly decrease myocardial infarction (MI) area, increase left ventricular ejection fraction (LVEF), and decrease cell death and pro-inflammatory cytokines in the serum. Decreased apoptosis and inflammatory cytokines were also observed in H/R cells after Lut treatment. Lut treatment downregulated SHP-1 expression and subsequently upregulated STAT3 phosphorylation in both I/R rat heart tissue and H9c2 cells. The findings of the current study suggest that Lut can protect the heart and reduce MI area, cell apoptosis rate, and inflammatory level in I/R models.

The fate of concomitant mild mitral regurgitation in aortic insufficiency: A neglected subject.

Objectives: Mitral regurgitation (MR) is commonly experienced by patients with aortic insufficiency (AI), and in its mild form, it is considered benign. However, the progression of concomitant mild regurgitation after the aortic valve surgery (AVS) for AI is poorly characterized. The current study aimed to define the long-term outcomes of MR after surgery and identify the risk factors involved in deterioration. Methods: Patients presenting with moderate/severe AI and concomitant mild MR (n = 347) between January 2013 and December 2021 were enrolled. MR grade was assessed by transthoracic echocardiography during the follow-up, and deterioration is defined as an increase in grade to moderate or severe MR from the previous follow-up echocardiography. Analysis of risk factors for early mortality, MR deterioration, and long-term mortality was performed. Results: A total of 278 patients (84.8%) among 328 survivors had at least one follow-up echocardiography, and complete follow-up occurred for 316 patients (96.3%). Mild MR improved to trivial or none in 194 patients (69.8%), progressed to persistent mild MR for 74 patients (26.6%), and deteriorated for 10 patients (3.6%). Preoperative atrial fibrillation [odds ratio (OR), 23.09; 95% confidence interval (CI), 4.35-122.54] and rheumatic AI (OR, 11.61; 95% CI, 1.26-106.85) were shown to be independent risk factors for MR deterioration by generalized linear mixed analysis. Conclusion: Progression of concomitant mild MR is rare in patients with AI after AVS. However, rheumatic AI and preoperative atrial fibrillation increase the probability of MR deterioration. Careful follow-up for this cohort of patients is recommended.

Current Surgical Management of Acute Type A Aortic Dissection in China: A Multicenter Registry Study.

Background: Many countries and regions have established multicenter registration studies to improve the outcomes of acute type A aortic dissection (ATAAD). Objectives: The aims of this study were to report actual preoperative management, surgery type, and early outcomes of surgical treatment for ATAAD in China. Methods: This cohort study uses data from the China Registry of Type A Aortic Dissection, a national clinical registry to investigate management of patients with Stanford type A aortic dissection. The data, including surgical management and outcomes of patients with ATAAD, were analyzed from January 2018 to December 2021. Results: A total of 1,058 patients with ATAAD were enrolled in this study between January 2018 and December 2021. The mean age of all patients was 51.6 ±11.7 years. The median interval from onset to hospital was 10.65 hours (IQR: 6-24 hours), and the median interval from entering the emergency room to starting operation was 13 hours (IQR: 4.08-28.7 hours). Total arch repair was performed in 938 patients (88.7%), and frozen elephant trunk repair was performed in 800 patients (75.6%). The incidence of early mortality was 7.6%. Conclusions: The population of patients with ATAAD in China experienced a longer interval from onset to arrival at the hospital, received more extensive aortic arch repair, and showed a relatively lower early mortality. These findings suggest that there may be a huge survivor bias in patients with ATAAD in China, more efforts should be made to promote prehospital emergency care and preoperative management of Chinese ATAAD patients. (A multicenter registration study of aortic dissection in China; ChiCTR1800015338).

MicroRNA-1278 ameliorates the inflammation of cardiomyocytes during myocardial ischemia by targeting both IL-22 and CXCL14.

AIMS: This study aimed to elucidate the role of microRNAs (miRNAs) during myocardial infarction (MI) development in vivo and in vitro. MAIN METHODS: Differentially expressed miRNAs between heart tissue from the MI mouse model and the control mouse were identified via microarray. Quantitative PCR (qPCR) and western blotting (WB) were performed to examine the expression levels of miRNAs and proteins, respectively. EdU-staining and colony formation assay were performed to assess cell viability and growth. Annexin V- and PI-staining-based flow cytometry was used to assess cell apoptosis. An MI mouse model was also established to study the function of miR-1278 in vivo. KEY FINDINGS: The levels of miR-1278 were reduced in the infarct regions of heart tissues of the MI mouse model and in H2O2-treated newborn murine ventricular cardiomyocytes (NMVCs) compared to those in the heart tissues of healthy mice and non-treated NMVCs. H2O2 treatment suppressed the proliferation of NMVCs, while miR-1278 upregulation improved it. Moreover, we found that miR-1278 inhibited the upregulation of IL-22 and CXCL14 expression in H2O2-treated NMVCs by directly binding with the 3'-UTRs of both IL-22 and CXCL14. Furthermore, restoration of IL-22 and CXCL14 in H2O2-treated NMVCs promoted miR-1278-induced inflammation and apoptosis. Administration of agomiR-1278 to the MI mouse model significantly improved cardiac activity. SIGNIFICANCE: Collectively, our findings illustrate that the expression of miR-1278 is low in H2O2-treated NMVCs and post-MI cardiac tissues, and the overexpression of miR-1278 in these protects against cell death by modulating IL-22 and CXCL14 expression.

Short-term outcomes of acute coronary involvement in type A aortic dissection without myocardial ischemia: a multiple center retrospective cohort study.

BACKGROUND: To evaluate the early prognosis and management of acute coronary involvement (ACI) in type A aortic dissection (ATAAD) patients without myocardial ischemia (MI). METHODS: We conducted a retrospective cohort study on a multicenter database. A total of 931 ATAAD patients without MI underwent thoracic aortic surgery between 2018 and 2019 in the Acute Aortic Syndrome Cooperation Network (AASCN) and were enrolled in our study. Patients were divided into two groups: ACI group and non-ACI group. RESULTS: There were 139 ACI patients (14.9%) and 792 non-ACI patients (85.1%) in our cohort. ACI group had higher 30-day mortality after surgery than non-ACI group (log-rank test: P = 0.028,Cox regression: hazard ratio [HR], 2.3; 95% confidence interval [95% CI], 1.1-5.39; P = 0.047), especially in sub-group of advanced age (53-80 years; HR, 4.0; 95% CI, 1.3-12.8; P = 0.017), low diastolic blood pressure (29-69 mmHg, HR, 3.8; 95% CI, 1.3-11.2; P = 0.018), low systolic blood pressure (51-119 mmHg, HR, 3.6; 95% CI, 1.1-12.4; P = 0.040), high body mass index (BMI;27.25-47.52 kg/m2; HR, 3.7; 95% CI, 1.3-10.7; P = 0.015) and high hemoglobin (>145 g/L; HR, 4.3; 95% CI, 1.2-16.0; P = 0.030). Acute renal failure was significant more in ACI group than non-ACI group (24.5% vs. 15.9%; P = 0.014). CONCLUSIONS: ACI increases the short-term postoperative mortality and acute renal failure in ATAAD patients without MI. ATAAD patients with ACI may need a narrower control range of blood pressure even if without myocardial ischemia. TRIAL REGISTRATION: ChiCTR1900022637 . Retrospectively registered 19 April 2019.

Machine Learning Prediction Model for Acute Renal Failure After Acute Aortic Syndrome Surgery.

BACKGROUND: Acute renal failure (ARF) is the most common major complication following cardiac surgery for acute aortic syndrome (AAS) and worsens the postoperative prognosis. Our aim was to establish a machine learning prediction model for ARF occurrence in AAS patients. METHODS: We included AAS patient data from nine medical centers (n = 1,637) and analyzed the incidence of ARF and the risk factors for postoperative ARF. We used data from six medical centers to compare the performance of four machine learning models and performed internal validation to identify AAS patients who developed postoperative ARF. The area under the curve (AUC) of the receiver operating characteristic (ROC) curve was used to compare the performance of the predictive models. We compared the performance of the optimal machine learning prediction model with that of traditional prediction models. Data from three medical centers were used for external validation. RESULTS: The eXtreme Gradient Boosting (XGBoost) algorithm performed best in the internal validation process (AUC = 0.82), which was better than both the logistic regression (LR) prediction model (AUC = 0.77, p < 0.001) and the traditional scoring systems. Upon external validation, the XGBoost prediction model (AUC =0.81) also performed better than both the LR prediction model (AUC = 0.75, p = 0.03) and the traditional scoring systems. We created an online application based on the XGBoost prediction model. CONCLUSIONS: We have developed a machine learning model that has better predictive performance than traditional LR prediction models as well as other existing risk scoring systems for postoperative ARF. This model can be utilized to provide early warnings when high-risk patients are found, enabling clinicians to take prompt measures.

Comparison of the efficacy and safety of thoracic endovascular aortic repair with open surgical repair and optimal medical therapy for acute type B aortic dissection: A systematic review and meta-analysis.

BACKGROUND: Current treatment approaches for acute type B aortic dissection (TBAD) are diversified. Thoracic endovascular aortic repair (TEVAR) as an effective and convenient intervention has been adopted extensively. However, the superior efficacy and safety of TEVAR have not yet been well evaluated. This meta-analysis was designed to comprehensively compare the efficacy and safety of TEVAR with open surgical repair and optimal medical therapy for acute type B aortic dissection. METHODS: A systematic search of PubMed, Embase, Cochrane Library and Web of Science up to April 1, 2020 was conducted for relevant studies that compared the efficacy of TEVAR and other conventional interventions in the treatment of TBAD. The primary outcomes were early mortality and midterm or long term survival. The secondary outcomes included early complications and other late outcomes. Two reviewers assessed trial quality and extracted the data independently. All statistical analyses were performed using the standard statistical procedures provided in Review Manager 5.2. RESULTS: A total of 18 studies including 12,789 patients were identified. 30-day/in-hospital mortality was significantly lower in TBAD patients with TEVAR than open surgical repair (OSR), with a pooled OR of 0.54 (95% CI 0.43-0.68; P < 0.00001). Compared with optimal medical therapy (OMT), TEVAR experienced lower incidence of long-term death (≥5-yr mortality), with a pooled OR of 0.46 (95% CI 0.24-0.86; P = 0.02). However, no significant difference between TEVAR and OSR or OMT in long-term survival was found. Compared with OSR, lower incidence of cardiac and pulmonary complications as well as shorter length of stay were observed in TEVAR. Compared with OMT, TEVAR showed higher rate of paraplegia or paraparesis, higher complete thrombosis of the false lumen, as well as longer length of ICU stay. CONCLUSIONS: Our analysis shows that TEVAR may be favorable in reducing 30-day/in-hospital mortality (than OSR) and long-term mortality (than OMT). TEVAR experienced equal efficacy with OSR and OMT in long-term survival. TEVAR showed higher rate of paraplegia or paraparesis, higher complete thrombosis of the false lumen, as well as longer length of ICU stay than OMT; and lower incidence of cardiac and pulmonary complications as well as shorter length of stay than OSR. However, TEVAR indicated similar incidence of other complications and outcomes with OSR and OMT. Further studies especially randomized clinical trials are needed to comprehensively compare the efficacy TEVAR.

The lncRNA H19/miR-675 axis regulates myocardial ischemic and reperfusion injury by targeting PPARα.

Increasing evidence has indicated that lncRNAs and miRNAs play important roles in the pathogenesis of myocardial ischemic and reperfusion (I/R) injury. This study investigated the potential roles and underlying molecular mechanisms of lncRNA H19 and H19-derived miR-675 in regulating myocardial I/R injury in vitro and in vivo. The results showed that expression of H19 and H19-derived miR-675 was upregulated in cardiomyocytes exposed to oxygen-glucose deprivation and reperfusion. Knockdown of H19 increased cell viability, reduced cell apoptosis, decreased inflammatory cytokines (IL-1ß, TNF-α and IL-6), inhibited oxidative stress, downregulated p-IκB-α and p-p65, and upregulated expression of Nrf2 and HO-1. All of these effects were partly reversed by overexpression of miR-675. Furthermore, we found that PPARα was a target gene of miR-675 and that H19 negatively regulated PPARα expression via miR-675. By inhibiting PPARα, the biological effects of miR-675 or H19 inhibition on cellular functions (apoptosis, inflammation and oxidative stress) were at least partially reversed. Moreover, knockdown of H19 significantly reduced infarct size, increased left ventricular systolic pressure, and decreased left ventricular end-diastolic pressure in a mouse model of myocardial I/R. Taken together, these data indicate that H19 inhibition protects the heart against myocardial I/R injury, which may be partly attributed to regulation of the miR-675/PPARα axis.

Influence of oxidized low density lipoprotein on the proliferation of human artery smooth muscle cells in vitro.

The effects of oxidized low density lipoprotein (ox-LDL) on the proliferation of cultured human vascular smooth muscle cells (vSMC) were investigated in vitro. By using NaBr density gradient centrifugation, LDL was isolated and purified from human plasma. Ox-LDL was produced from LDL by being incubated with CuSO(4). ox-LDL was then added to the culture medium at different concentrations (35, 60, 85, 110, 135 and 160 microg/mL) for 7 days. The influence of ox-LDL on vSMC proliferation was observed in growth curve, mitosis index, and in situ determination of apoptosis. The data were analyzed with SPSS 10.0 software. The results showed that the ox-LDL produced in vitro had a good purity and optimal oxidative degree, which was similar to the intrinsic ox-LDL in atherosclerotic plaque. ox-LDL at a concentration of 35 microg/mL demonstrated the strongest proliferation inducement, and at a concentration of 135 microg/mL, ox-LDL could inhibit the growth of vSMC. ox-LDL at concentrations of 35 and 50 microg/mL presented powerful mitotic trigger, and with the increase of ox-LDL concentration, the mitotic index of vSMC was decreased gradually. ox-LDL at higher concentrations promoted more apoptotic vSMCs. ox-LDL at lower concentrations triggered proliferation of vSMCs, and at higher concentrations induced apoptosis in vSMCs. ox-LDL played a promotional role in the pathogenesis and development of atherosclerosis by affecting vSMC proliferation and apoptosis.