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Dilated cardiomyopathy (DCM) is a common cause of heart failure. However, genetic-level treatments are not available for this condition. In this study, we searched for biological markers and therapeutic targets for DCM from a genetic perspective. We chose microarray datasets of idiopathic DCM with heart failure tissues and normal function (NF) heart tissues, which were downloaded from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) were analyzed by the GEO2R tool. Gene ontology (GO) and gene set enrichment analysis were used to analyze the functions of DEGs and the pathways in which they are involved. Next, protein-protein interaction networks were built to filter out the hub genes from DEGs. The expression of hub gene was validated by other GEO datasets. Receiver operating characteristic (ROC) curves were plotted to verify the accuracy of the genetic diagnosis. In the end, the mRNA-miRNA-lncRNA network was built to find potentially correlative genes. Twenty-eight common DEGs in total were screened, and GO analysis showed that DEGs were mainly associated with neutrophil degranulation and activation, regulation of Wnt signaling pathway and the development of cardiac cell and tissue. Five hub genes (asporin [ASPN], osteoglycin [OGN], secreted frizzled-related protein 4 [SFRP4], membrane metalloendopeptidase [MME], and natriuretic peptide gene [NPPA]) were shown to be highly expressed in the validation sets and accurate in distinguish between DCM and NF by ROC curves. miRNA prediction of the hub genes revealed that hsa-mir-28b-5p was associated with SFRP4, ASPN, and MME. All of them may serve as biological diagnostic indicators and provide direction for treatment at the genetic level.

Background Increasingly, the shared risk factors and pathological processes of atherosclerosis and abdominal aortic aneurysm (AAA) are being recognized. However, the exact mechanism underlying the shared pathogenesis of atherosclerosis and AAA formation remains unclear. Methods The aim of our study was to identify the hub genes involved in the pathogenesis of atherosclerosis and AAA. Our analysis was based on two gene expression profiles for atherosclerosis (GSE28829) and AAA (GSE7084), downloaded from the Gene Expression Omnibus (GEO) database. Common differential genes were identified and an enrichment analysis of differential genes was conducted, with construction of protein-protein interaction networks, and identification of common hub genes and predicted transcription factors. Results The analysis identified 133 differentially expressed genes (116 upregulated and 17 downregulated), with the enrichment analysis identifying a potential important role of integrins and chemokines in the common immune and inflammatory responses of atherosclerosis and AAA. Regulation of the complement and coagulation cascades and regulation of the actin cytoskeleton were associated with both diseases, with 10 important hub genes identified: TYROBP, PTPRC, ITGB2, ITGAM, PLEK, CTSS, LY86, ITGAX, CCL4, and FCER1G. Conclusions Findings identified a common pathogenetic pathway between atherosclerosis and AAA, with integrin-related genes playing a significant role in both diseases. The common pathways and hub genes identified provide new insights into the shared mechanisms of these two diseases and can contribute to identifying new therapeutic targets and predicting the therapeutic effect of biological agents.

Background: Blood urea nitrogen (BUN) and serum albumin (SA) are related to mortality in patients with cardiovascular diseases, such as acute aortic dissection. However, there are no data on the relationship between BUN-to-albumin ratio (BA-R) and mortality in patients with acute type A aortic dissection (ATAAD). Thus, the aim of this study was to evaluate the prognostic value of BA-R for the prediction of in-hospital mortality in patients who underwent emergency surgery for ATAAD.Methods: Patients who were diagnosed with ATAAD and underwent emergency surgery within 48 h of onset at our hospital between January 2015 and December 2021 were included in this study. The primary endpoint of this study was postoperative in-hospital mortality (POIM). The data of the survivors and non-survivors were retrospectively compared. Univariate and multivariable logistic regression analyses were performed to investigate the association between BA-R and POIM.Results: A total of 557 patients with ATAAD were enrolled in this study. Of these, 505 survived and 52 did not. The preoperative BA-R of the non-survivor group was significantly higher than that of the survivor group (0.27 [0.18, 0.46] vs. 0.12 [0.10, 0.16] mmol/g; P < 0.001). Univariate regression analysis showed that preoperative BA-R ≥0.155 mmol/g, serum creatinine level ≥96.3 µmol/mL, SA level Conclusion: Preoperative BA-R is a simple, rapid, and potentially useful prognostic indicator of POIM in patients with ATAAD.

Objective: To evaluate the efficacy of sacubitril/valsartan for the treatment of patients with chronic heart failure (CHF) after cardiac valve surgery (CVS).Methods: Data of 259 patients who underwent CVS due to organic heart disease, and who were admitted to the hospital with CHF from January 2018 to December 2020, were collected. The patients were divided into Group A (treatment with sacubitril/valsartan) and Group B (treatment without sacubitril/valsartan). The duration of treatment and follow-up was 6 months. Prior-treatment clinical characteristics, post-treatment data, mortality, and follow-up data of the two groups were analyzed.Results: The total effective rate of Group A was higher than that of Group B (82.56% versus 65.52%, P < 0.05). The left ventricular ejection fraction (LVEF) was improved in both groups (11.14 ± 10.16 versus 7.15 ± 11.18, P = 0.004). The left ventricular end-diastolic/-systolic diameter (LVEDD/LVESD) in Group A decreased more than that in Group B (3.58 ± 9.21 versus 0.27 ± 14.44, P=0.026; 4.21 ± 8.15 versus 1.14 ± 12.12, P=0.016, respectively). The N-terminal prohormone of B-type natriuretic peptide (NT-proBNP) in both groups decreased (1305.65 ± 2000.85 versus 675.91 ± 1649.84, P=0.012). The systolic and diastolic blood pressure (SBP/DBP) in Group A decreased more than that in Group B (13.13 ± 23.98 versus 1.81 ± 10.89, P < 0.001; 8.28 ± 17.79 versus 2.37 ± 11.41, P = 0.005, respectively). Liver and renal insufficiency, hyperkalemia, symptomatic hypotension, Angioedema or acute heart failure have no statistical differences between the two groups.Conclusion: Sacubitril/valsartan can effectively improve the cardiac function of CHF patients after CVS by increasing LVEF, reducing LVEDD, LVESD, NT-proBNP and BP, with good safety.

Objective: To evaluate the perioperative clinical efficacy of preoperative human fibrinogen treatment in patients with acute Stanford type A aortic dissection (ATAAD).Methods: Data of 159 patients with ATAAD who underwent emergency surgical treatment in our hospital from January 2019 to December 2020 were retrospectively analyzed. Patients were divided into two groups according to whether human fibrinogen was administered before surgery. The preoperative clinical data, surgical data, postoperative data, complications related to the coagulation function, and mortality of the two groups were compared and analyzed.Results: The in-hospital mortality was similar in the two groups (2.9% versus 9.3%, P = 0.122). However, group A had a significantly shorter operation time (279.24±39.03 versus 298.24±45.90, P=0.008), lower intraoperative blood loss (240.48±96.75 versus 353.70±189.80, P＜0.001), and reduced intraoperative transfusion requirement of red blood cells (2.61±1.18 versus 6.05±1.86, P＜0.001). The postoperative suction drainage within 24 hours in group A was significantly decreased (243.24±201.52 versus 504.22±341.08，P=0.002). The incidence of postoperative acute kidney injury (AKI) in group A was lower than that in group B (3.8% versus 14.8%, P =0.023). Similarly, the incidence of postoperative hepatic insufficiency in group A was lower than that in group B (1.9% versus 9.3%, P =0.045). In group A, the mechanical ventilation time was shorter (47.68±28.61 versus 118.21±173.16, P=0.004) along with reduced ICU stay time (4.06±1.18 versus 8.09±9.42, P=0.003), and postoperative hospitalization days (19.20±14.60 versus 23.50±7.56, P=0.004).Conclusion: Preoperative administration of human fibrinogen in patients undergoing ATAAD surgery can effectively reduce the intraoperative blood loss, blood transfusion amount, shorten the operation time, reduce postoperative complications, and improve the early prognosis of patients, in addition to being highly safe.

Background: Triosephosphate isomerase 1 (TPI1) is a crucial enzyme in glycolysis/gluconeogenesis and has been associated with a variety of diseases. However, there is little information on TPI1 and aortic aneurysms (AA). This study was designed to reveal the association between TPI1 and aortic aneurysms, and the mechanisms underlying TPI1 activity in AAs. Methods: Tandem Mass Tag (TMT)-based Liquid chromatography mass spectrometry/mass spectrometry (LC-MS/MS) and the Mann-Whitney test were used to compare variables between AA and normal aortic tissues. Gene ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were analyzed using Fun-Rich software. The expression of the TPI1 protein in human aortic tissues was verified by Western blotting. A mouse AA model was established by infusing Ang-II for 4 weeks, then the expression of TPI1, SM22, α-SMA, OPN and MMP2/9 proteins were evaluated by western blotting. TPI1 overexpression was achieved by transfection of TPI mRNA, and its effect on gene expression was studied by RT-qPCR and western blotting, which included SM22, α-SMA, OPN, and MMP2/9. Ang II-induced expression of TPI1 and phenotypic-related genes in VSMCs. Results: TPI1 is closely related to the glycolysis/gluconeogenesis pathway and is higher in AA. Expression of TPI1 was upregulated in AA aortic samples of both human and mouse models, p

The efficacy of primary sutureless repair for supracardiac total anomalous pulmonary venous connection (TAPVC) needs to be confirmed. This study aimed to compare the long-term outcomes between the conventional surgery and the sutureless technique with a modified approach in superior TAPVC. Between January 2008 and December 2018, 173 patients with supracardiac TAPVC underwent surgery either with the conventional procedure (n = 130) or the sutureless repair (n = 43). Multivariate analysis and competing-risk analysis were used to identify risk factors for early death and postoperative pulmonary venous obstruction (PVO), respectively. Among 173 patients who underwent repair of supracardiac TAPVC, 46 (28%) had preoperative PVO, and 22 (12.7%) had postoperative PVO. The sutureless group had a lower postoperative PVO rate compared with the conventional group (p = 0.027). The risk factors for death were age ≤ 28 days [odds ratio (OR), 11.56; 95% confidence interval (CI) 1.33–100.47, p = 0.015], weight ≤ 3 kg (OR 9.57; 95% CI 1.58–58.09, p = 0.009), emergency operation (OR 19.24; 95% CI 3.18–116.35, p = 0.002), cardiopulmonary bypass time (OR 2.16; 95% CI 1.36–3.43, p = 0.003), cross-clamp time (OR 1.73; 95% CI 1.20–2.50, p = 0.022), and duration of ventilation (OR 1.11; 95% CI 1.02–1.21, p = 0.027). Age ≤ 28 days [Hazard Ratio (HR) 1.92; 95% CI 1.92–11.02, p

Objectives The partial upper sternotomy (PUS) approach is acceptable for aortic valve replacement, and even aortic root operation. However, the efficiency of PUS for extensive arch repair of acute type A aortic dissection (AAAD) in older adult patients has not been well investigated. Methods Between January 2014 and December 2019, 222 older adult patients (≥ 65 years) diagnosed with AAAD went through extensive arch repair, among which 127 received PUS, and 95 underwent full sternotomy (FS). Logistic regression analysis was used to identify risk factors for early death, and negative binomial regression analysis was applied to explore risk factors related to post-operative ventilator-supporting time and intensive care unit stay time. Results Total early mortality was 8.1% (18/222 patients). The PUS group had shorter Cardiopulmonary bypass time (133.0 vs.155.0 min, P P P P = 0.012) and malperfusion syndromes (OR 65.83; 95% CI 11.53–375.86; P P = 0.003), when compared with the FS group. Conclusions The early results of emergency extensive arch repair of AAAD via PUS in older adult patients were satisfactory. However, the long-term results remain to be investigated.

BackgroundCorticosteroids can effectively inhibit systemic inflammation induced by cardiopulmonary bypass. Recently clinical trials and meta-analyses and current guidelines for cardiac surgery do not support corticosteroids prophylaxis during cardiac surgery because of an increase in myocardial infarction and no benefit for patients. The aim of this study is to determine whether specific corticosteroids dose ranges might provide clinical benefits without increasing myocardial infarction.MethodsThe PubMed, Web of Science, Embase, Clinical Trials, and Cochrane databases were searched for randomized controlled trials (RCTs) published before August 1, 2021.Results88 RCTs with 18,416 patients (17,067 adults and 1,349 children) were identified. Relative to placebo and high-dose corticosteroids, low-dose corticosteroids (≤20 mg/kg hydrocortisone) during adult cardiac surgery did not increase the risks of myocardial infarction (odds ratio [OR]: 0.96, 95% confidence interval [CI]: 0.43–2.17; p = 0.93). However, low-dose corticosteroids were associated with lower risks of atrial fibrillation (OR: 0.58, 95% CI: 0.44–0.76; p p = 0.04). Furthermore, low-dose corticosteroids significantly shortened the mechanical ventilation times (mean difference [MD]: −2.74 h, 95% CI: −4.14, −1.33; p = 0.0001), intensive care unit (ICU) stay (MD: −1.48 days, 95% CI: −2.73, −0.22; p = 0.02), and hospital stay (MD: −2.29 days, 95% CI: −4.51, −0.07; p = 0.04).ConclusionLow-dose corticosteroids prophylaxis during cardiac surgery provided significant benefits for adult patients, without increasing the risks of myocardial infarction and other complications.

Background miR‐145 is closely related to vascular smooth muscle cells (VSMC) phenotype transformation; however, the regulatory mechanisms through which miR‐145 regulates the VSMC phenotype transformation under mechanical stretching are unclear. In this study, we evaluated the roles of miR‐145 in VSMCs subjected to mechanical stretching in aortic dissection (AD). Methods The expression of miR‐145 in the aortic vessel wall of model animals and patients with AD was analyzed by quantitative polymerase chain reaction. miR‐145‐related protein‐protein interaction networks and Wikipathways were used to analyze VSMC phenotypic transformation pathways regulated by miR‐145. We used gain‐ and loss‐of‐function studies to evaluate the effects of miR‐145 on VSMC differentiation under mechanical stretch induction and assessed whether Krüppel‐like factor 4 (KLF4) was regulated by miR‐145 in the aorta under mechanical stretch conditions. Results miR‐145 was abundantly expressed in the walls of the normal human aorta, but was significantly downregulated in animal models and the walls of patients with dissection. We found that contractile phenotype‐related proteins were downregulated in VSMCs subjected to mechanical stretching, whereas the expression of secreted phenotype‐related proteins increased. miR‐145 overexpression also downregulated contractile phenotype‐related proteins in VSMCs and suppressed upregulation of phenotype‐related proteins. Finally, under mechanical stretching, KLF4 expression was significantly increased in VSMCs, and overexpression of miR‐145 blocked this effect. Conclusion Our results confirmed that mechanical stretch‐induced phenotypic transformation of VSMCs to promote AD via upregulation of KLF4; this mechanism was regulated by miR‐145, which directly modulated KLF4 expression and VSMC differentiation., miR‐145 was abundantly expressed in the walls of the normal human aorta, but was significantly downregulated in animal models and the walls of patients with dissection. Contractile phenotype‐related proteins were downregulated in VSMCs subjected to mechanical stretching, whereas the expression of secreted phenotype‐related proteins increased. Mechanical stretch induced phenotypic transformation of VSMCs to promote AD via upregulation of KLF4. This mechanism was regulated by miR‐145, which directly modulated KLF4 expression and VSMC differentiation.

This study sought to investigate the differentially expressed miRNAs in Aortic dissection (AD) and explore the downstream mechanisms in regulating AD.Exosomes of AD patients and healthy people were isolated by differential centrifugation, and the differentially expressed miRNAs were evaluated by RNA sequencing. The downstream target of miR-222-3p was predicted by bioinformatics method and validated by dual-luciferase assay. Angiotensin II and Promethazine were used to establish AD mouse model and platelet-derived growth factor BB (PDGF-BB) was used to induce human vascular smooth muscle cells (HVSMCs) to elucidate the effect of miR-222-3p upregulation on AD in vivo and in vitro. The relative level of miR-222-3p was evaluated by RT-qPCR. The level of several proteins was investigated by Western blot. Immunofluorescence staining was used to detect the stress fiber formation. Cell migration was evaluated by wound healing and Transwell assay. The proliferation, cell cycle and apoptosis of HVSMCs were assessed by CCK-8 and flow cytometry, respectively.MiR-222-3p was downregulated in AD and PDGF-BB induced HVSMCs. The upregulation of miR-222-3p alleviated the symptom of AD in vivo by targeting STAT3, and inhibited stress fiber formation, abnormal migration, proliferation and apoptosis of HVSMCs induced by PDGF-BB by regulating the expression of α-SMA, SM22α, MMP2, MMP9 and p-Smad2.The upregulation of miR-222-3p attenuates the progression of AD. Our study provides a theoretical basis for exploring new strategies against AD.

Herein we described a novel repair approach for a left atrial esophageal fistula. Complete mediastinal debridement and simultaneous primary repairs of the left atrial posterior wall and the esophagus were completed under a median sternotomy, central cardiopulmonary bypass, left atrial circular incision around four pulmonary veins, inflamed left atrial posterior wall removal, and posterior pericardial opening.

Background: Hepatic dysfunction (HD) is a serious complication after cardiovascular surgery. However, risk factors of developing hepatic dysfunction after acute type A aortic dissection (AAAD) are largely unclear. Methods: The clinical data of 227 patients with AAAD repaired by modified triple-branched stent graft implantation from January 2018 to January 2020 were collected retrospectively, including preoperative , surgical and postoperative information. Logistics regression was used to explore the potential risk factors of HD. Results: In the early stage after operation, a total of 57 patients were complicated with HD, accounting for 25.11%. The hospital mortality rate in these patients with HD was 19.30%, while the rate in patients without HD was only 6.5%. We found that preoperative body mass index (BMI)>30kg/㎡(OR: 7.054, 95%CI: 1.798-27.678, P=0.005), preoperative renal insufficiency(OR:7.575,95%CI:2.923-19.629, P=0.000),preoperative moderate/severe pericardial effusion(OR: 16.409, 95%CI: 2.81-93.444, P=0.002) and cardiopulmonary bypass time>180min (OR: 7.190, 95%CI: 3.113-16.608, P＝0.000) were independent risk factors for HD after AAAD repaired by modified triple-branched stent graft implantation. Conclusions: Preoperative BMI>30kg/㎡, preoperative renal insufficiency, preoperative moderate/severe pericardial effusion and cardiopulmonary bypass time>180min are independent risk factors for HD after total arch repair with modified triple-branched stent graft implantation in AAAD patients. And the occurrence of HD after operation would prolong the time of mechanical ventilation and the hospitalization time of ICU, and significantly increase the in-hospital mortality of patients. Keywords: risk factors,acute type A aortic dissection,hepatic dysfunction, modified triple-branched stent graft implantation, total arch repair

Hypertension is a key risk factor for spontaneous coronary artery dissection (SCAD) and aortic dilation. Circulating proteins play key roles in a range of biological processes and represent a major source of druggable targets. The aim of this study was to identify circulating proteins that were associated with blood pressure (BP), SCAD and aortic dilation. We identified shared genetic variants of BP and SCAD in genome-wide association studies, searched for circulating protein affected by these variants and examined the association of circulating protein levels with BP, aortic aneurysm and dissection (AAD) and aortic diameters by integrating data from circulating protein quantitative trait loci (pQTL) studies and genome wide association study (GWAS) in individuals from the UK Biobank using two-sample Mendelian randomization analysis methods. Single nucleotide polymorphisms (SNPs) in JAG1, ERI1, ULK4, THSD4, CMIP, COL4A2, FBN1, FAM76B, FGGY, NUS1, and HNF4G, which were related to extracellular matrix components, were associated with both BP and SCAD. We found 49 significant pQTL signals among these SNPs. The regulated proteins were encoded by MMP10, IL6R, FIGF, MMP1, CTSB, IGHG1, DSG2, TTC17, RETN, POMC, SCARF2, RELT, and GALNT16, which were enriched in biological processes such as collagen metabolic process and multicellular organism metabolic process. Causal associations between BP and AAD and aortic diameters were detected. Significant associations between circulating levels of cathepsin B, a well-known prorenin processing enzyme, and BP and aortic diameters were identified by using several Mendelian randomization analysis methods and were validated by independent data.ConclusionThe present study identified the association between circulating cathepsin B and BP and aortic diameters. The findings indicated that BP-associated genetic variants may influence aortic dilation risk by circulating proteins that regulate BP.

The main strategy of tissue repair and regeneration focuses on the application of mesenchymal stem cells and cell-based nanoparticles, but there are still multiple challenges that may have negative impacts on human safety and therapeutic efficacy. Cell-free nanotechnology can effectively overcome these obstacles and limitations. Mesenchymal stem cell (MSC)-derived natural small extracellular vesicles (sEVs) represent ideal nanotherapeutics due to their low immunogenicity and lack of tumorigenicity. Here, sEVs harvested from Wharton's jelly mesenchymal stem cells (WJMSCs) were identified. In vitro results showed that WJMSC-sEVs efficiently entered chondrocytes in the osteoarthritis (OA) model, further promoted chondrocyte migration and proliferation and modulated immune reactivity. In vivo, WJMSC-sEVs notably promoted chondrogenesis, which was consistent with the effect of WJMSCs. RNA sequencing results revealed that sEV-microRNA-regulated biocircuits can significantly contribute to the treatment of OA, such as by promoting the activation of the calcium signaling pathway, ECM-receptor interaction pathway and NOTCH signaling pathway. In particular, let-7e-5p, which is found in WJMSC-sEVs, was shown to be a potential core molecule for promoting cartilage regeneration by regulating the levels of STAT3 and IGF1R. Our findings suggest that WJMSC-sEV-induced chondrogenesis is a promising innovative and feasible cell-free nanotherapy for OA treatment.

BackgroundThe mid-term and long-term efficacies of valve preservation in acute DeBakey I aortic dissection (AD) are controversial. Thus, it is unclear whether middle-aged patients with acute DeBakey I AD should undergo modified valve-sparing procedures or the Bentall procedure in an emergency setting.MethodsThis study included 213 middle-aged Chinese patients (under 60 years old) who were treated for acute DeBakey I AD between January 2009 and June 2015. The treatments involved modified valve-sparing aortic root replacement (VSARR) (117 patients) or the Bentall procedure (96 patients). Preoperative, intraoperative, postoperative, and follow-up data were analyzed. Echocardiography and thoracoabdominal computed tomography angiography (CTA) findings were reviewed at 3 months, 1 year, and then annually after surgery.ResultsNo significant differences were observed in terms of the preoperative, intraoperative, in-hospital mortality, and postoperative parameters. There were also no significant differences in aortic regurgitation (AR). However, follow-up examinations using CTA revealed that 6 patients had endoleakage at the distal end of the triple-branched stent (0/110 patients [0.0%] vs. 6/90 patients [6.7%],P = 0.022). The anticoagulation-related thromboembolism/bleeding events was significantly lower in group A than in group B (0/110 patients [0.0%] vs. 11/90 patients [11.1%],P = 0.001). And postoperative aortic valve re-operation rate was significantly lower in group A (1/110 patients [0.9%] vs. 8/90 patients [8.9%],P = 0.020). There was no significant difference in survival during the follow-up period (log-rankP > 0.05).ConclusionFor middle-aged patients with acute DeBakey I AD, VSARR were associated with a lower rate of endoleakage at the distal end of the triple-branched stent, thromboembolism/bleeding events and aortic valve re-operation (vs. the Bentall procedure).

Background: Circulating low-density lipoprotein cholesterol (LDL-C) plays a causal role in coronary artery disease (CAD). However, genetic risk factors of CAD were not yet fully understood. The aim of the study was to identify additional factors that contributed to CAD.Methods: We conducted integrative analysis on publicly available data from genome-wide association studies and quantitative trait locus studies by employing two-sample Mendelian randomization methods to examine the associations of gene expression and circulating protein levels with LDL-C and CAD.Results: We found that mRNA expression levels of SORT1, PSRC1 and CELSR2 in liver cells were significantly associated with both LDL-C and CAD (P < 5.0 × 10-8). Higher expression levels of SORT1, PSRC1 and CELSR2 in the liver were significantly associated with lower circulating LDL-C level (beta= -0.142, -0.138 and -0.171, respectively) and CAD risk (beta= -0.10, -0.097 and -0.121, respectively). Expression levels of 31 genes in blood cells associated with LDL-C level were found. Expressions of PSRC1, IL6R, GGCX, VAMP8, LIPA, NT5C2, SWAP70, EIF2B2, FURIN, FES and ATP5G1 in blood cells were significantly associated with CAD. Higher circulating granulins and apolipoprotein B levels, which were strongly affected by PSRC1 and APOB variants, were significantly associated with higher LDL-C level (beta = 0.22 and 1.35) and CAD risk, with odds ratios of 1.15 (1.10-1.19) and 1.45 (1.21-1.74), respectively. Conclusions: This study identified gene expressions in liver and blood cells and circulating granulins and apolipoprotein B that were genetically associated with LDL-C and CAD and provided evidence for exploring the potential causal relationship.

Background Although corticosteroid prophylaxis in adult cardiac surgery has been studied extensively for 40 years, its role remains controversial, and the optimal dose remains uncertain. The objective of this meta-analysis was to estimate the clinical benefits and risks of corticosteroid use in cardiopulmonary bypass. Methods We will search Pubmed, Web of Science, Embase, Clinical Trials, and Cochrane Central Register of Controlled Trials for relevant clinical trials published in any language before August 1, 2020. Randomized controlled trials (RCTs) of interest which meet inclusion criteria published or unpublished will be included. We will divide the included studies into child and adult groups for analysis. If sufficient data are available, the included trials will be divided into 4 subgroups: ≤20 mg/kg (low dose), 20-40 mg/kg (slightly high dose), 40-100 mg/kg (high dose), and >100 mg/kg (ultra high dose) based on the equivalent hydrocortisone dose. INPLASY registration number: INPLASY2020100044. Results The results of this study will be published in a peer-reviewed journal. Conclusion This study will compare the efficacy of tprophylactic corticosteroids for adults and children undergoing cardiac surgery with CPB. Due to the nature of the disease and intervention methods, randomized controlled trials may be inadequate, and we will carefully consider inclusion in high-quality, non-randomized controlled trials, but this may result in high heterogeneity and affect the reliability of the results.

Background: The mid-term and long-term efficacies of valve preservation in acute DeBakey I aortic dissection(AD) are controversial. Thus, it is unclear whether middle-aged patients with acute DeBakey I AD should undergo valve-sparing procedures or the Bentall procedure in an emergency setting.Methods: This study included 213 middle-aged Chinese patients(30-60 years old) who were treated for acute DeBakey I AD between January 2009 and June 2015. The treatments involved valve-sparing aortic root replacement(VSARR)(117 patients) or the Bentall procedure(96 patients). Preoperative, intraoperative, postoperative, and follow-up data were analyzed. Echocardiography and thoracoabdominal computed tomography angiography(CTA) findings were reviewed at 3 months, 1 year, and then annually after surgery. Results: No significant differences were observed in terms of the preoperative, intraoperative, in-hospital mortality, and postoperative parameters. There were also no significant differences in aortic regurgitation(AR). However, follow-up examinations using CTA revealed that 6 patients had endoleakage at the distal end of the triple-branched stent(0/110 patients [0.0%] vs. 6/90 patients [6.7%], P=0.022). The anticoagulation-related thromboembolism/bleeding events was significantly lower in group A than in group B(0/110 patients [0.0%] vs. 11/90 patients [11.1%], P=0.001). And postoperative aortic valve re-operation rate was significantly lower in group A (1/110 patients [0.9%] vs. 8/90 patients [8.9%], P=0.020). There was no significant difference in survival during the follow-up period (log-rank P>0.05).Conclusion: For middle-aged patients with acute DeBakey I AD, VSARR were associated with a lower rate of endoleakage at the distal end of the triple-branched stent, thromboembolism/bleeding events and aortic valve re-operation(vs. the Bentall procedure) .

Background We developed an integrated triple-branched stent to treat acute DeBakey type I aortic dissection (AD) and modified it to enhance its adaptability. However, whether the patients treated by the modified stent would achieve better long-term prognosis is unknown. Methods This study enrolled 147 patients with acute DeBakey type I AD. The original integrated triple-branched stents were used in 57 patients (Group A) between July 2012 and August 2013, and the modified stents in 90 patients (Group B) between September 2013 and March 2015. Clinical characteristics, surgical data, postoperative complications, mortality, and follow-up data of the two groups were analyzed. Results The two groups presented comparable early death rates (Group A = 7.0%, Group B = 5.9%; p = .719). The incidence of postoperative acute kidney injury (AKI) was lower in Group B (10.0%) versus Group A (24.6%) (p = .018). Compared with the original integrated triple-branched stent graft, the modified stent could reduce the risk of early postoperative AKI (OR [95% CI] = 0.36 [0.14, 0.94]). Early endoleak rates were significantly lower in Group B (1.0%) compared to Group A (9.4%) (p = .004). During follow-up, there were five deaths in Group A (9.4%) and six deaths in Group B (7.2%) (p = .646). Chronic kidney injury (7.5% vs. 3.6%; p = .311), delayed endoleak (11.3% vs. 4.8%; p = .157), and late reinterventions (7.5% vs. 2.4%; p = .155) in the two groups were similar. Conclusions In patients with acute DeBakey type I AD, the modified stent showed feasible and safe treatment outcomes and reduced early endoleak rates. However, the long-term effects were similar to the original treatment.

Background We studied early poor postoperative prognosis in acute Stanford type A aortic dissection (ATAAD) patients and investigated the predictive effect of interleukin-6 (IL-6) combined with D-dimer in the early poor postoperative prognosis after ATAAD. Methods Data on 141 ATAAD patients, who underwent emergency surgery between January 2018 and December 2018 at our hospital, were studied. We analyzed early postoperative prognosis using two patient groups. Patients with good prognosis were included in group A and those with poor prognosis were in group B. Univariate logistic and multivariable logistic regression analysis were performed for poor early postoperative prognosis. Results Preoperative IL-6 level was lower (57.8 ± 39.0 vs 211.0 ± 153.7 pg/mL, p p 108 pg/mL (area under the curve: AUC = 0.901) and D-dimer > 14.0 μg/mL (AUC = 0.817). Univariate logistic regression analysis showed that IL-6 > 108 pg/mL, D-dimer > 14.0 μg/mL, prothrombin time > 15 s, creatinine > 135 mmol/mL, and operation time > 306 min for ATAAD appeared to be early postoperative risk factors of poor prognosis. Multivariable logistic regression analysis showed that IL-6 > 108 pg/mL and D-dimer > 14.0 μg/mL were early postoperative risk factors for poor prognosis after ATAAD, and the odds ratios (ORs) of IL-6 > 108 pg/mL and D-dimer > 14.0 μg/mL were 24.937 (6.837, 90.931) and 18.757 (5.094, 69.075), respectively. When IL-6 was > 108 pg/mL (AUC = 0.901), the sensitivity and specificity of predicting early postoperative prognosis after ATAAD were 79.4 and 89.7%, respectively (95% confidence interval [CI] 0.839 to 0.963). When D-dimer was > 14.0 g/mL (AUC = 0.817), the sensitivity and specificity were 82.4 and 84.1%, respectively (95% CI 0.731 to 0.903). When combined with D-dimer (AUC = 0.936) (95% CI 0.793 to 0.979), the AUC values were more predictive than those for the individual marker. Conclusion IL-6 > 108 pg/mL and D-dimer > 14.0 μg/mL is of high predictive value for the assessment of early poor postoperative prognosis after ATAAD. And IL-6 > 108 pg/mL in combination with D-dimer > 14.0 μg/mL is of higher predictive value.