Expression of CCL2 signaling pathway genes in patients with periodontitis and atherosclerosis.

OBJECTIVE: Periodontitis and atherosclerosis are chronic inflammatory diseases characterized by leukocyte infiltration. We investigated the expression of CCL4, CCR5, c-Jun, c-Fos, NF-κB, and CCL2 as well as the possible mechanism involved in the regulation of CCL2 in human periodontitis tissues and atherosclerotic aorta based on previous research on the CCL4/CCR5/c-Jun and c-Fos/CCL2 pathway leading to CCL2 expression in collagen-induced arthritis (CIA) rat. METHODS: Sixty-five volunteers were recruited and the condition of their gingiva and coronary arteries were assessed. The subjects were divided into four groups: healthy control, chronic periodontitis (CP), coronary artery diseases (CAD), and noncoronary artery diseases (non-CAD). Total RNA was isolated from gingiva in periodontitis patients and control populations and from the aorta in patients with and without CAD. PCR was used to examine CCL4, CCR5, c-Jun, c-Fos, NF-κB, and CCL2 levels. The production of CCL2 in the gingiva and aorta was analyzed by immunostaining. RESULTS: PCR revealed that CCL4, CCR5, and CCL2 mRNA levels were increased in CP patients' gingivae and aortas from coronary artery bypass grafting (CABG) patients. Marked c-Jun, c-Fos, and NF-κB gene productions were detected in CP patients' gingivae but did not show statistical differences between the CAD and non-CAD groups. Stronger immunoreactivity against CCL2 was observed in periodontitis gingiva and aorta from CABG patients. CONCLUSIONS: Our findings suggest that the CCL4/CCR5/c-Jun and c-Fos/CCL2 pathways may be involved in CCL2 expression in periodontitis. CCL4, CCR5, and CCL2 might act as possible nodes to link the presence of periodontitis and atherosclerosis.

Identification of important genes related to HVSMC proliferation and migration in graft restenosis based on WGCNA.

The great saphenous vein is the most commonly used vessel for coronary artery bypass grafting (CABG), but its use has been associated with a high restenosis rate at 10-year follow-up. This study sought to determine the key genes associated with vein graft restenosis that could serve as novel therapeutic targets. A total of 3075 upregulated and 1404 downregulated genes were identified after transcriptome sequencing of three pairs of restenosed vein grafts and intraoperative spare great saphenous veins. Weighted gene co-expression network analysis showed that the floralwhite module had the highest correlation with vein graft restenosis. The intersection of the floralwhite module gene set and the upregulated gene set contained 615 upregulated genes strongly correlated with vein graft restenosis. Protein-protein interaction network analysis identified six hub genes (ITGAM, PTPRC, TLR4, TYROBP, ITGB2 and CD4), which were obtained using the STRING database and CytoHubba. Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses showed that the common hub genes were mainly involved in the composition of the cell membrane; in biological processes such as neutrophil degranulation, receptor binding and intercellular adhesion, innate immune deficiency; and other signaling pathways. Finally, ITGB2 was selected as the target gene, and its expression was verified in tissues. The results showed that ITGB2 was significantly overexpressed in occluded vein grafts. To study the function of ITGB2 in HVSMCs, primary HVSMCs were cultured and successfully identified. EdU incorporation, wound healing and transwell assays showed that ITGB2 silencing significantly inhibited the proliferation and migration of HVSMCs stimulated by PDGF-BB. Overall, our study provides a basis for future studies on preventing restenosis following CABG.

Clinical characteristics of autoimmune encephalitis with co-existence of multiple anti-neuronal antibodies.

BACKGROUND: An increasing number of cases of autoimmune encephalitis (AE) with co-existing multiple anti-neuronal antibodies have been reported in recent years. However, the clinical significance of the concurrent presence of multiple anti-neuronal antibodies in patients with AE remains unclear. METHODS: We retrospectively enrolled AE patients with multiple anti-neuronal antibodies treated at our center between August 2019 and February 2022. We also reviewed cases reported in multiple literature databases. Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline was followed on selection process. And then the clinical and laboratory data of these cases were collected for review and summary. RESULTS: A total of 83 AE cases with multiple antibodies (9 cases from our center and 74 cases from the literatures reviewed) were identified. In our center, nine patients presented with encephalitis symptoms, clinically characterized as disturbed consciousness, seizures, cognitive impairment, and psychiatric disorders. Of the 83 cases, 73 cases had co-existence of 2 types of antibodies, 8 cases had 3 types, and 2 cases had 4 types. Thirty-nine cases (39/83, 46.9%) were confirmed or suspected of also having a tumor, of which the most common was lung cancer (28/83, 33.7%). Partial or complete recovery was achieved in 57 cases (57/83, 68.6%), while 26 cases (26/83, 31.3%) died during treatment or follow-up. CONCLUSIONS: AE with co-existing multiple anti-neuronal antibodies is a specific subgroup, that is increasingly recognized in clinical practice. The co-existence of multiple anti-neuronal antibodies has a major impact on clinical features, disease progression, and prognosis.

NDUFB11 and NDUFS3 regulate arterial atherosclerosis and venous thrombosis: Potential markers of atherosclerosis and venous thrombosis.

Atherosclerosis is a chronic disease that thickens the blood vessel walls and narrows the lumen. Venous thrombosis is a blood clot that forms in the body's deep veins or pulmonary arteries. However, the relationship between NDUFB11 and NDUFS3 and atherosclerosis and venous thrombosis is unclear. We employed data files that combined atherosclerosis and chronic stress groups. Subsequently, we conducted differential gene expression analysis (DEGs) and performed weighted gene co-expression network analysis (WGCNA). We constructed and analyzed a protein-protein interaction (PPI) network. Further analyses included functional enrichment analysis, gene set enrichment analysis (GSEA), gene expression heatmaps, immune infiltration analysis, and mRNA analysis. By comparing our findings with the Comparative Toxicogenomics Database (CTD), we identified the most relevant diseases associated with the core genes. Additionally, we utilized TargetScan to screen for miRNAs regulating the central DEGs. To validate our results, we conducted Western Blot experiments at the cellular level. A total of 1747 DEGs were co-identified. According to the Gene Ontology (GO) analysis of differentially expressed genes, they were primarily enriched in mitochondrial gene expression, mitochondrial envelope, organelle membrane, and mitochondrial inner membrane categories. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that the target cells were mainly enriched in metabolic pathways, ribosomes, and histidine metabolism. The intersection of enriched terms from both GO and KEGG analyses showed significant enrichment in mitochondrial gene expression, mitochondrial envelope, organelle inner membrane, ribosomal structural constituents, histidine metabolism, and oxidative phosphorylation. Eight core genes were identified, including NDUFS5, UQCRQ, COX6C, COX7B, ATP5ME, NDUFS3, NDUFA3, and NDUFB11. The gene expression heatmap demonstrated that core genes (NDUFB11 and NDUFS3) were downregulated in atherosclerosis with venous thrombosis samples and upregulated in normal samples. CTD analysis revealed that the core genes NDUFB11 and NDUFS3 were associated with pain, arterial diseases, atherosclerosis, arteritis, venous thrombosis formation, and venous thromboembolism. We added Western Blot basic cell experiment for verification. NDUFB11 and NDUFS3 are downregulated in atherosclerosis and venous thrombosis, associated with poorer prognosis, and may serve as potential biomarkers for both diseases.

NDUFB11 and NDUFS3 play a role in atherosclerosis and chronic stress.

OBJECTIVE: Atherosclerosis is characterized by the formation of fibrofatty plaques in the intima of arteries, resulting in thickening of the vessel wall and narrowing of the lumen. Chronic stress refers to individuals in a state of long-term chronic stress. However, the relationship between NDUFB11 and NDUFS3 and atherosclerosis and chronic stress is unclear. METHOD: The atherosclerosis with chronic stress group data file was used. DEGs were screened and WGCNA was performed. Construction and analysis of PPI Network. Functional enrichment analysis, GSEA, gene expression heatmap, immune infiltration analysis and mRNA analysis were performed. CTD was used to find diseases most related to core genes. WB was performed. TargetScan was used to screen miRNAs of DEGs. RESULTS: 1708 DEGs were identified. According to GO analysis, they were mainly enriched in catabolic processes, organic acid metabolism processes, carboxylic acid metabolism processes. KEGG analysis showed that they were mainly enriched in metabolic pathways, fatty acid metabolism, pentose phosphate pathway, glycolysis / gluconeogenesis, fructose and mannose metabolism. Gene expression heatmap showed that the core genes (NDUFB11, NDUFS3) were lowly expressed in samples of those with atherosclerosis accompanied by chronic stress and highly expressed in the normal samples. NDUFB11 and NDUFS3 were associated with necrosis, hyperplasia, inflammation, renal disease, weight loss, memory impairment, and cognitive impairment. WB showed that the expression level of NDUFS3 in atherosclerosis and chronic stress was lower than that in control group. CONCLUSIONS: NDUFB11 and NDUFS3 are underexpressed in atherosclerosis and chronic stress; the lower NDUFB11 and NDUFS3 levels, the worse the prognosis.

Ninety-seven cases of experiences with the left thoracotomy approach for off-pump conventional revascularization: a retrospective cohort study.

Background: Minimally invasive coronary surgery-coronary artery bypass grafting (MICS CABG) is well adopted in clinical practice. However, this procedure did not really achieve conventional complete revascularization. The present study aimed to explore the feasibility and safety of conventional revascularization via the left thoracotomy (8-10 cm) approach. Methods: From January 2020 to March 2022, a total of 97 consecutive patients who needed coronary artery revascularization were operated on using this technique. The patients' preoperative, intraoperative, postoperative, and follow-up data were collected. Perioperative variables were compared between the single graft and non-single graft groups. All patients received dual-source computerized tomographic angiography at 1-week postoperatively to evaluate the graft patency and detect pulmonary embolism and aortic dissection. The patients were followed up for 3-27 months. Results: The mean age of the entire cohort was 61.5±8.8 years, there were 16 (16.5%) female patients, and 1-4 grafts were performed per patient. There were no conversions to median sternotomy or on-pump CABG. The average number of grafts was 1.9±0.9, and that of the non-single graft group was 2.5±0.6. Among the 97 included patients, one patient in the single graft group suffered from aspiration pneumonia after a stroke and died. The 30-day mortality was 1.0% (one patient), one patient required re-exploration for bleeding (1.1%), and a total of 191 grafts were performed. All grafts were unobstructed except for one graft to the obtuse marginal branch (OM) (0.5%). Follow-up was performed by phone or via outpatient visits and was available for 92 patients (95%). During the follow-up period, 1 (1.1%) patient suffered an acute myocardial infarction and received percutaneous coronary intervention with no redo-surgery. All patients are alive and angina-free. Conclusions: Left thoracotomy for conventional revascularization is a safe procedure for appropriately selected patients, with few early complications and good early and mid-term results. More cases are ongoing and long-term results are in observation.

Integrated proteomic and metabolomic profile analyses of cardiac valves revealed molecular mechanisms and targets in calcific aortic valve disease.

Background: This study aimed to define changes in the metabolic and protein profiles of patients with calcific aortic valve disease (CAVD). Methods and results: We analyzed cardiac valve samples of patients with and without (control) CAVD (n = 24 per group) using untargeted metabolomics and tandem mass tag-based quantitative proteomics. Significantly different metabolites and proteins between the CAVD and control groups were screened; then, functional enrichment was analyzed. We analyzed co-expressed differential metabolites and proteins, and constructed a metabolite-protein-pathway network. The expression of key proteins was validated using western blotting. Differential analysis identified 229 metabolites in CAVD among which, 2-aminophenol, hydroxykynurenine, erythritol, carnosine, and choline were the top five. Proteomic analysis identified 549 differentially expressed proteins in CAVD, most of which were localized in the nuclear, cytoplasmic, extracellular, and plasma membranes. Levels of selenium binding protein 1 (SELENBP1) positively correlated with multiple metabolites. Adenosine triphosphate-binding cassette transporters, starch and sucrose metabolism, hypoxia-inducible factor 1 (HIF-1) signaling, and purine metabolism were key pathways in the network. Ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), calcium2+/calmodulin-dependent protein kinase II delta (CAMK2D), and ATP binding cassette subfamily a member 8 (ABCA8) were identified as hub proteins in the metabolite-protein-pathway network as they interacted with ADP, glucose 6-phosphate, choline, and other proteins. Western blotting confirmed that ENPP1 was upregulated, whereas ABCA8 and CAMK2D were downregulated in CAVD samples. Conclusion: The metabolic and protein profiles of cardiac valves from patients with CAVD significantly changed. The present findings provide a holistic view of the molecular mechanisms underlying CAVD that may lead to the development of novel diagnostic biomarkers and therapeutic targets to treat CAVD.

Successful management of a combined cardiopulmonary penetrating injury: a case report.

Background: Penetrating thoracic injury is a type of critical illness with a high mortality rate, which often involves the heart, large blood vessels, and lungs. Penetrating cardiac injury is a very serious condition, and most patients die rapidly within minutes due to hemorrhagic shock and acute cardiac tamponade. Due to the critical condition and rapid development of this type of injury, most patients die before reaching the hospital. It is rare in clinical practice and difficult to treat. Case Description: Our hospital recently admitted a case of penetrating cardiac injury. In this case, a 50-year-old male was admitted to the hospital following "a fall from a height [that] caused steel bar[s] to penetrate the chest cavity for 7 hours before he arrived at the hospital". The patient fell from a height of 3meters at a construction site, which caused 2 steel bars to penetrate his chest. The patient presented with symptoms such as chest pain, dyspnea, and apathy. Chest computed tomography suggested combined cardiopulmonary penetrating injury. Echocardiography suggested penetrating cardiac injury, and moderate pericardial effusion. After the patient was sent to the Emergency Department of our hospital, the relevant laboratory examinations and an emergency surgery were performed. The rescue team consisting of cardiac surgery, thoracic surgery, anesthesiology, emergency department, and imaging department specified the treatment plan. Under general anesthesia, cardiopulmonary bypass was performed via right femoral arteriovenous cannulation. The steel bars were removed, the left atrial posterior wall and ventricular septal perforation were repaired, and the great cardiac vein was sutured. Coronary artery bypass surgery was performed at the same time, and the anterolateral lung tissue of the left lower lobe was resected. Postoperative treatment was given to prevent against infection and improve cardiopulmonary function. The patient recovered well, and he was discharged from the hospital. The results of the follow-up 1 year after surgery were normal. Conclusions: Timely treatment and a reasonable operation mode is essential in treating this kind of trauma. A joint diagnosis and treatment by a multidisciplinary team can enable a comprehensive assessment of the condition to be made quickly and an optimal treatment plan to be formulated.

Transcriptomics Reveals the Effect of Thymol on the Growth and Toxin Production of Fusarium graminearum.

Fusarium graminearum is a harmful pathogen causing head blight in cereals such as wheat and barley, and thymol has been proven to inhibit the growth of many pathogens. This study aims to explore the fungistatic effect of thymol on F. graminearum and its mechanism. Different concentrations of thymol were used to treat F. graminearum. The results showed that the EC50 concentration of thymol against F. graminearum was 40 µg/mL. Compared with the control group, 40 µg/mL of thymol reduced the production of Deoxynivalenol (DON) and 3-Ac-DON by 70.1% and 78.2%, respectively. Our results indicate that thymol can effectively inhibit the growth and toxin production of F. graminearum and cause an extensive transcriptome response. Transcriptome identified 16,727 non-redundant unigenes and 1653 unigenes that COG did not annotate. The correlation coefficients between samples were all >0.941. When FC was 2.0 times, a total of 3230 differential unigenes were identified, of which 1223 were up-regulated, and 2007 were down-regulated. Through the transcriptome, we confirmed that the expression of many genes involved in F. graminearum growth and synthesis of DON and other secondary metabolites were also changed. The gluconeogenesis/glycolysis pathway may be a potential and important way for thymol to affect the growth of F. graminearum hyphae and the production of DON simultaneously.

Risk factors for delirium after coronary artery bypass grafting in elderly patients.

BACKGROUND: Postoperative delirium (POD) is a common complication of major surgery and is associated with fortified morbidity, mortality, and long-term cognitive dysfunction. This study sought to evaluate the incidence and risk factors of delirium in elderly (aged ≥65 years) patients who underwent coronary artery bypass grafting (CABG). METHODS: We performed a retrospective cohort analysis. The clinical data of 1,426 elderly patients who underwent CABG at our hospital from October 2018 to October 2020 were collected and analyzed. Delirium was defined as any positive Confusion Assessment Method for Intensive Care Unit examination following surgery during the intensive care unit (ICU) stay. Risk factors for POD were authenticated via univariate and multivariate logistic regression analyses. The intraoperative and postoperative factors were evaluated using a propensity score-matched regression analysis based on preoperative factors. RESULTS: A total of 39.3% (560 of 1,426) of elderly patients who underwent CABG were diagnosed with delirium. Based on the multivariate analysis, age [odds ratio (OR) 1.013], long-term alcohol consumption (OR 2.026), diabetes (OR 1.51), stroke (OR 1.41), and extracardiac arteriopathy (OR 1.61) were found to be independent predictors of post-cardiac surgery delirium. Conversely, high-density lipoprotein cholesterol levels (HDL-C) ≥1.0 mmol/L (OR 0.71) was found to be a protective factor. Among the intraoperative and postoperative factors evaluated, only a prolonged ICU stay (≥48 h; OR 1.62) was identified as a risk factor for developing delirium in the propensity-score matched analysis, after adjusting for potential confounding variables and selection bias. In contrast to the earlier analysis, the multivariate logistic regression further revealed that peri-procedural myocardial infarction and postoperative arterial oxygen partial pressures were not significantly associated with POD. CONCLUSIONS: The incidence of POD in elderly patients undergoing CABG was high. Factors such as older age, long-term alcohol consumption, diabetes, stroke, and extracardiac arteriopathy were independent risk factors for POD in these patients. In relation to the intraoperative and postoperative factors, after adjusting for preoperative confounding factors, only a prolonged ICU stay was identified as a risk factor for POD. Additionally, high levels of HDL-C may be beneficial in reducing the incidence of delirium.

BPI and KIR6.1 as significant hub genes for vein graft restenosis.

BACKGROUND: Vein graft restenosis (VGR), which appears to be caused by dyslipidemia following vascular transplantation, seriously affects the prognosis and long-term quality of life of patients. METHODS: This study analyzed the genetic data of restenosis (VGR group) and non-stenosis (control group) vessels from patients with coronary heart disease post-vascular transplantation and identified hub genes that might be responsible for its occurrence. GSE110398 was downloaded from the Gene Expression Omnibus database. A repeatability test for the GSE110398 dataset was performed using R language. This included the identification of differentially expressed genes (DEGs), enrichment analysis via Metascape software, pathway enrichment analysis, and construction of a protein-protein interaction network and a hub gene network. RESULTS: Twenty-four DEGs were identified between VGR and control groups. The four most important hub genes (KIR6.1, PCLP1, EDNRB, and BPI) were identified, and Pearson's correlation coefficient showed that KIR6.1 and BPI were significantly correlated with VGR. KIR6.1 could also sensitively predict VGR (0.9 < area under the curve ≤1). CONCLUSION: BPI and KIR6.1 were differentially expressed in vessels with and without stenosis after vascular transplantation, suggesting that these genes or their encoded proteins may be involved in the occurrence of VGR.

Ubiquitin-specific protease as the underlying gene biomarker for aortic stenosis.

BACKGROUND: Aortic stenosis is a common heart valvular disease whose pathological processes include an inflammatory reaction and lipid accumulation. However, its detailed pathogenesis is yet to be completely elucidated. Therefore, it is of great significance to further explore the molecular mechanisms of aortic stenosis. METHODS: Four datasets were downloaded from the Gene Expression Omnibus (GEO) database. Firstly, the differently expressed genes (DEGs) were screened between control and aortic stenosis samples. Secondly, weighted gene co-expression network analysis (WGCNA) was performed to find the highly relevant gene modules. Enrichment analysis and protein-protein interaction (PPI) networking were also performed, then Cytoscape was used to identify hub genes. Finally, the six participants (3 control participants and 3 patients with aortic stenosis) were recruited at the Tianjin Chest Hospital. In order to verify the expression level of USP14, several molecular experiments were performed, including hematoxylin-eosin (HE) staining, immunohistochemistry, immunofluorescence technology, real time-quantitative polymerase chain reaction (RT-qPCR), and western blotting. RESULTS: A total of 9636 DEGs were found between the control and aortic stenosis samples. The DEGs were mainly enriched in the autophagy-animal, cellular lipid catabolic process, apoptosis, and glycoside metabolic process categories. Eleven hub genes were identified via four different algorithms. Following verification of the patient samples, Ubiquitin-specific protease 14 (USP14) was found to be displayed at higher levels in the aortic stenosis samples. CONCLUSION: USP14 might be involved in the occurrence and development of aortic stenosis, so it would be a molecular target for early diagnosis and specific treatment of aortic stenosis. There is a significant association between the high expression of USP14 and aortic stenosis, indicating that this gene may be a genetic risk factor for aortic stenosis.

Preliminary study of the application of transthoracic echocardiography-guided three-dimensional printing for the assessment of structural heart disease.

OBJECTIVE: To investigate the feasibility and diagnostic value of a preoperative transthoracic echocardiography-guided three-dimensional printed model (TTE-guided 3DPM) for the assessment of structural heart disease (SHD). METHODS: Fourty-four patients underwent cardiac surgery at Tianjin Chest Hospital. The patients were preoperatively assessed using TTE-guided 3DPM, which was compared to conventional three-dimensional transthoracic echocardiography (3DTTE) along with direct intraoperative findings, which were considered the "gold standard." Twelve patients had SHD, including four with mitral prolapse, two with partial endocardial cushion defects, two with secondary atrial septal defects, two with rheumatic mitral stenosis, one with tetralogy of Fallot, and one with a ventricular septal defect (VSD). Thirty-two patients who did not have SHDs were designated as the negative control group. RESULTS: The sensitivity and specificity of the TTE-guided 3DPM were greater than or equal to those of the 3DTTE. The P-value of the McNemar test of 3DTTE was >.05, which indicates that the difference was not statistically significant (Kappa = 0.745, P < .001). The P-value of the McNemar test of TTE-guided 3DPM was >.05, which indicates that the difference was not statistically significant (Kappa = 0.955, P < .001). A comparison of 3DTTE and TTE-guided 3DPM resulted in a P-value >.05, which indicates that the difference was not statistically significant (Kappa = 0.879, P < .001). TTE-guided 3DPM displayed the 3D structure of SHDs and cardiac lesions clearly and was consistent with the intra-operative findings. CONCLUSION: Transthoracic echocardiography-guided three-dimensional printed model (TTE-guided 3DPM) provides essential information for preoperative evaluation and decision making for patients with SHDs.

Performance of EuroSCORE II and SinoSCORE in Chinese patients undergoing coronary artery bypass grafting.

OBJECTIVES: The European System for Cardiac Operative Risk Evaluation II (EuroSCORE II) was developed to update EuroSCORE and incorporated refinement and modification of several risk factors. SinoSCORE was designed by Chinese scholars based on 9839 patients who underwent coronary artery bypass grafting (CABG) at 43 participating institutions. This study was designed to validate the EuroSCORE II and SinoSCORE in Chinese patients undergoing CABG and to compare their performance overall and per subgroup. METHODS: A total of 4507 adult receiving CABG at our institution between January 2010 and April 2014 were included in this retrospective study. Patients were stratified for cardiovascular risk using EuroSCORE II and SinoSCORE. The performance of EuroSCORE II and SinoSCORE was analysed with a focus on discrimination power and calibration. RESULTS: The in-hospital mortality rate for the entire cohort was 1.4%, while the mortality rate predicted by EuroSCORE II was 1.47 ± 1.2% (95% CI 1.43-1.50) and by SinoSCORE was 2.86 ± 3.5% (95% CI 2.76-2.96). The C-statistics of EuroSCORE II and SinoSCORE were 0.728 and 0.716, respectively. The Hosmer-Lemeshow test indicated that EuroSCORE II had poor goodness of fit while SinoSCORE performed slightly better. When patients were divided into quartiles based on predicted risk, respectively defined as group I, II, III and IV, EuroSCORE II underestimated mortality rates of patients scored IV, but overestimated mortality rates in all other groups; SinoSCORE underestimated mortality rates of patients scored I and overestimated mortality rates in all other groups. EuroSCORE II only achieved good discrimination for patients scored I (area under the receiver operating characteristic curve, AUC = 0.707 > 0.70), and SinoSCORE achieved poor discrimination for all subgroups except group II (AUC = 0.754 > 0.70). EuroSCORE II overestimated the mortality rate in the isolated CABG group and underestimated mortality rates in patients with other cardiac surgeries. SinoSCORE overestimated mortality rates in all pathology subgroups. The AUC values of EuroSCORE II and SinoSCORE were 0.694 and 0.687, respectively, for isolated CABG. The AUC values of EuroSCORE II and SinoSCORE were 0.772 and 0.669 for combined cardiac surgery CABG. CONCLUSIONS: EuroSCORE II could predict mortality in the entire group and in the low-middle risk group, but not in the high-risk group, in which it underestimated mortality. SinoSCORE overestimated mortality rates in the entire group and in all subgroups. Risk models should be targeted to different heart diseases, and the statistical methods of established risk systems should be improved.

Percutaneous Catheter Drainage in Infected Pancreatitis Necrosis: a Systematic Review.

The primary aim of this study was to present the outcomes of percutaneous catheter drainage (PCD) in patients with infected pancreatitis necrosis. A second aim was to focus on disease severity, catheter size, and additional surgical intervention. A literature search of the PubMed/MEDLINE/Cochrane Library (January 1998 to February 2015) databases was conducted. All randomized, non-randomized, and retrospective studies with data on PCD techniques and outcomes in patients with infected pancreatitis necrosis were included. Studies that reported data on PCD along with other interventions without the possibility to discriminate results specific to PCD were excluded. The main outcomes were mortality, major complications, and definitive successful treatment with percutaneous catheter drainage alone. Fifteen studies of 577 patients were included. There was only one randomized, controlled trial, and most others were retrospective case series. Organ failure before PCD occurred in 55.3 % of patients. With PCD alone, definitive successful treatment was 56.2 % of patients. Additional surgical intervention was required after PCD in 38.5 % of patients. The overall mortality rate was 18 % (104 of 577 patients). Complications occurred in 25.1 % of patients, and fistula was the most common complication. PCD is an efficient tool for treatment in the majority of patients with infected pancreatitis necrosis as the only intervention. Multiple organ failures before PCD are negative parameters for the outcome of the disease. Large catheters fail to prove to be more effective for draining necrotic tissue. However, in the extent of multi-morbid patients, to determine one single prognostic factor seems to be difficult.

Collagenous fibroma of the right coronary cusp: a case report and literature review.

Collagenous fibroma (desmoplastic fibroblastoma) is a rare benign tumor. This type of tumor mostly occurs in the subcutaneous tissues or skeletal muscle, and to the best of our knowledge, there is no unique case report of it occurring in the cardiac valves. This is the first description of collagenous fibroma in a human heart.

Fibrous cyst of the chordae tendineae of the mitral valve: echocardiographic appearance and literature review.

Fibrous cyst of the chordae tendineae of the mitral valve (MV) is defined as a fibrous cyst arising from the chordae tendineae of the MV. It is extremely rare and its etiology is not clear. We present a case of a cystic structure within the left ventricle. This structure is connected to the anterior MV leaflet and the posterior chordae tendineae. It moves freely, resulting in stenosis of inflow tract and outflow tract of the left ventricle. Intraoperative assessment and histopathologic examination revealed it as a fibrous cyst. Its echocardiographic appearance is unique and it must be resected immediately.

The significance of natriuretic peptide in treatment of pulmonary hypertension after mitral valve replacement.

OBJECTIVES: To compare the therapeutic efficacy of recombinant human brain natriuretic peptide and prostaglandin E1 in the treatment of pulmonary hypertension after mitral valve replacement. METHODS: Sixty patients with postoperative pulmonary hypertension were divided randomly into 3 groups that received saline, prostaglandin E1, and natriuretic peptide infusions for 12 hours each. The hemodynamics data were monitored consecutively, and the levels of thromboxane A2 and cyclic guanosine monophosphate were detected pretreatment, after treatment, and 1 week after surgery. RESULTS: The arterial pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure decreased 1 hour after prostaglandin E1 treatment and rebounded after treatment discontinuation. The pulmonary arterial pressure and pulmonary capillary wedge pressure in the natriuretic peptide group decreased 3 hours after treatment; pulmonary arterial pressure decreased less than that of the prostaglandin group, and there was no evidence of hemodynamic rebound after treatment discontinuation. The natriuretic peptide had no significant effects on arterial pressure. In both the prostaglandin and natriuretic peptide groups, cyclic guanosine monophosphate increased after the treatment, which was even higher in the latter group. Prostaglandin E1 could lead to the decrease of thromboxane A2, which was not seen in the natriuretic peptide group. CONCLUSIONS: Both brain natriuretic peptide and prostaglandin E1 can effectively reduce pulmonary hypertension; however, natriuretic peptide has a slower and milder efficacy. The effects of these 2 drugs in reducing the pulmonary arterial pressure may be mediated through different pathways.

[Histopathologic features of degenerative aortic valve and its mechanisms].

OBJECTIVE: To explore the related pathogenesis of degenerative aortic valvular disease by observing the histopathological changes of aortic valves from patients with aortic degenerative stenosis and compare the results with those controls with normal aortic valves. METHODS: Between May 2009 and May 2010, 22 cases of degenerative calcified aortic valves from patients with aortic valve stenosis undergoing aortic valve replacement (14 males, 8 females, mean age: (66 ± 6) years) and 6 cases of normal aortic valves from those with dissection undergoing Bentall operation (4 males, 2 females, mean age: (43 ± 5) years) were collected. The results of hematoxylin and eosin staining and immunohistochemical examinations were used to observe the histological features of degenerative aortic valves and elucidate the related pathogenesis of degenerative aortic valvular disease. RESULTS: Degenerative aortic valve leaflets became thickened. Calcification appeared in aortic side of valve leaflets. Inflammatory infiltrate, angiogenesis, cholesterol crystals, foamy cell aggregation, diffuse and nodular calcification could be seen in subendocardial space of degenerative aortic valve leaflets. No expression of Osterix (OSX) or nuclear factor of activated T-cells 1 (NFATc1) was observed in normal valves. In contrast, the expressions of OSX and NFATc1 showed nuclear immunostaining in degenerative aortic valves. Immunohistochemical staining was graded from 0 to 3. And the expression of OSX was present in 1(4.5%), 1(4.5%), 8(36.4%) and 12 cases (54.5%) respectively in calcified areas, that of OSX in 4(18.2%), 6(27.3%), 7 (31.8%) and 5 cases (22.7%) respectively in non-calcified areas, that of NFATc1 in 1 (4.5%), 1 (4.5%), 8 (36.4%) and 12 cases (54.5%) respectively in calcified areas, that of NFATc1 in 4 (18.2%), 6 (27.3%), 8 (36.4%) and 4 cases (18.2%) respectively in non-calcified areas. The expressions of OSX and NFATc1 in calcified areas were higher than those in non-calcified areas (χ(2) = 8.320, P = 0.040 and χ(2) = 9.371, P = 0.025 respectively). CONCLUSIONS: Unlike in normal valves, inflammatory infiltrate, lipid deposition, angiogenesis and bone regulatory factors appear in degenerative aortic valves. And inflammatory infiltrate, lipid deposition, angiogenesis and ossification may be involved in the degenerative calcified aortic stenosis.