Association of Controlling Nutritional Status Score With Adverse Outcomes in Patients With Coronary Artery Disease: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis sought to examine the association between the controlling nutritional status (CONUT) score and adverse outcomes in patients with coronary artery disease (CAD). PubMed and Embase databases were searched for eligible studies from their inceptions to December 12, 2021 to identify studies investigating the association of the CONUT score with major adverse cardiovascular events (MACEs) and all-cause mortality in CAD patients. Twelve studies (36,198 CAD) patients satisfied the criteria. Comparison of the high with low CONUT score, the pooled multivariate adjusted risk ratios (RR) was 1.78 (95% confidence intervals [CI] 1.36-2.32) for MACEs and 1.45 (95% CI 1.27-1.66) for all-cause mortality, respectively. When compared with patients with normal nutrition, malnourished (defined by the CONUT score ≥2) patients conferred a 52% increased risk of MACEs. Additionally, per point CONUT score increment was associated with 15% and 11% higher risk of MACEs and all-cause mortality, respectively. Higher CONUT score independently predicts the MACEs all-cause mortality in CAD patients. Estimation of nutritional status using the CONUT score could be helpful for improving risk classification of CAD.

Associations of bisphenol F and S, as substitutes for bisphenol A, with cardiovascular disease in American adults.

Bisphenol A (BPA) exposure may be positively associated with cardiovascular disease (CVD). For more than a past decade, exposure to bisphenol F (BPF) and bisphenol S (BPS), as substitutes for BPA, has gradually increased in the population. Whether BPF and BPS exposure are associated with CVD remains unclear. We used data from the United States National Health and Nutrition Examination Survey (NHANES) from 2013 to 2016. A total of 3,502 participants, including 368 with CVD, were enrolled in the final analysis. Associations of BPA, BPF and BPS with CVD were determined using multivariate logistic regression analysis. The highest level of urinary BPA (≥2.5 ng/ml) was significantly associated with a higher CVD prevalence (odds ratio [OR], 1.58; 95% confidence interval [CI], 1.08-2.3) among all participants in the quartile analysis. In stratified analyses, the highest level of urinary BPA was positively associated with CVD prevalence in males (1.86, 1.1-3.13) and the elderly population (≥60 years old) (1.89, 1.2-2.97). Higher levels of urinary BPF were positively associated with CVD prevalence in females (Q2: 1.81, 1.03-3.18; Q4: 1.73, 1.07-2.79) and in the elderly population (Q3: 1.7, 1.16-2.48). No associations were found between urinary BPS levels and CVD, regardless of whether the participants were stratified by age or sex. In conclusion, exposure to BPA or BPF was positively correlated with CVD prevalence, but an association was not found for exposure to BPS. BPF may not be as safe as assumed for human health.

Coronary artery bypass on survival in patients with moderate ischemic mitral regurgitation: meta-analysis.

OBJECTIVE: The objective of the study was to systematically evaluate the effect of coronary artery bypass grafting (CABG) or CABG combined with mitral valve surgery (cMVS) on post-operative survival in patients with moderate ischemic mitral valve regurgitation. MATERIALS AND METHODS: Databases including PubMed, Web of Science, COCHRANE LIBRARY, WanFang Data, and CNKI Data were searched from inception to January 2020. According to the inclusion criterion, relevant articles were screened. After that we extracted data, assessed quality, and performed meta-analysis using RevMan 5.2. RESULTS: A total of 4 randomized controlled trial and 14 retrospective study involving 4476 patients were included in the study. The CABG group was 2278 and the cMVS group was 1698. The results of meta-analysis showed that compared with CABG group, there were no statistically significant differences in the recent mortality (odds ratio [OR] = 0.88, p = 0.62), 1-year survival (OR = 1.03, p = 0.82), 1-year survival (OR = 1.07, p = 0.62), and long-term survival (OR = 0.95, p = 0.61) of the cMVS group. CONCLUSION: Current evidence indicates that patients in the cMVS group did not benefit from CABG group in survival after surgery.

OBJETIVO: . Evaluar sistemáticamente el efecto del injerto de derivación de la arteria coronaria (CABG) o el injerto de derivación de la arteria coronaria combinados con la cirugía de la válvula mitral (cMVS) sobre la supervivencia posoperatoria en pacientes con insuficiencia valvular mitral isquémica moderada. MATERIAL Y MÉTODOS: . Se realizaron búsquedas en bases de datos que incluyen Pubmed, Web of Science, COCHRANE LIBRARY, WanFang Data y CNKI Data desde el inicio hasta enero de 2020. De acuerdo con el criterio de inclusión, se seleccionaron los artículos relevantes. Después de eso, extrajimos los datos, evaluamos la calidad y realizamos el metanálisis con RevMan 5.2. RESULTADOS: . Se incluyó un total de 4 ensayos controlados aleatorios (ECA) y 14 estudios retrospectivos con 4476 pacientes. El grupo CABG fue 2278, el grupo cMVS fue 1698. Los resultados del metanálisis mostraron que, en comparación con el grupo CABG, no hubo diferencias estadísticamente significativas en la mortalidad reciente (OR = 0.88, p = 0.62), supervivencia a 1 año (OR = 1.03, p = 0.82), supervivencia a 1 año (OR = 1.07, p = 0.62) y supervivencia a largo plazo (OR = 0.95, p = 0.61) del grupo cMVS. CONCLUSIÓN: . La evidencia actual indica que los pacientes del grupo cMVS no se beneficiaron del grupo CABG en la supervivencia después de la cirugía.

Identification of important genes related to ferroptosis and hypoxia in acute myocardial infarction based on WGCNA.

Acute myocardial infarction (AMI) tends to cause severe heart failure and the population suffering from AMI gradually become younger. This study aims to determine the key genes associated with AMI, ferroptosis and hypoxia that could serve as novel biomarkers for AMI. There were 522 up-regulated genes and 119 down-regulated genes in GSE4648. Based on the expression of ferroptosis-related genes (FRGs) and hypoxia-related genes, the ferroptosis Z-score and the hypoxia Z-score calculated by ssGSEA were significantly higher in the infarcted area of AMI mice than in the control group, and there was a positive correlation between ferroptosis and hypoxia Z-score. 6 modules were obtained by Weighted Gene Co-Expression Network Analysis (WGCNA), and 2 key modules and 66 key genes were screened out. Genes in the key modules were found mainly related to ERK1 and ERK2 cascade, TNF signaling pathway, and MAPK signaling pathway through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Protein-protein interaction (PPI) network analysis was performed on the key genes and 10 hub genes (Atf3, Ptgs2, Cxcl1, Socs3, Hspa1b, Selp, Cxcl2, Il1b, Myd88, and S100a8) were obtained using STRING and Cytohubba. The expression of 9 hub genes except Cxcl1 was consistent in GSE4648 and GSE775. The transcription factors (TFs)-hub genes interaction network was constructed and 48 TFs were obtained using TRRUST. Finally, it was verified through the animal experiment that these hub genes were up-regulated in AMI mice myocardial tissues. This study offers new ideas for the diagnosis and treatment of AMI.

Hypoxia-induced miR-27 and miR-195 regulate ATP consumption, viability, and metabolism of rat cardiomyocytes by targeting PPARγ and FASN expression.

This study examined whether hypoxia-induced microRNA (miRNA) upregulation was related to the inhibition of chondriosome aliphatic acid oxidation in myocardial cells under anoxia. We showed that anoxia induced high expression of hypoxia-inducible factor-1-alpha, muscle carnitine palmitoyltransferase I, and vascular endothelial growth factor in cardiomyocytes. Meanwhile, miR-27 and miR-195 were also upregulated in hypoxia-induced cardiomyocytes. Furthermore, hypoxia induction led to reductions in the adenosine triphosphate (ATP) consumption rate and oxidative metabolism as well as an increase in cardiomyocyte glycolysis. Metabolic reprogramming was reduced by hypoxia, as evidenced by the downregulation of sirtuin 1, forkhead box protein O1, sterol regulatory element-binding protein 1c, ATP citrate lyase, acetyl-coenzyme A carboxylase 2, adiponutrin, adipose triglyceride lipase, and glucose transporter type 4, while miR-27 and miR-195 inhibition partially recovered the expression of these transcription factors. In addition, hypoxia induction reduced cell viability and survival by triggering apoptosis; however, miR-27 and miR-195 inhibition partially increased cell viability. Moreover, miR-27 and miR-195 targeted the 3'untranslated regions of two key lipid-associated metabolic players, peroxisome proliferator-activated receptor gamma and fatty acid synthase. In conclusion, miR-27 and miR-195 are related to hypoxia-mediated ATP levels, glycolysis, oxidation, cell survival, and a cascade of transcription factors that control metabolism in cardiomyocytes.

The expression of Nesprin-1 increased in aortic dissection: why?

BACKGROUND: To detect the expression of Nesprin-1 in aortic dissection (AD) in patients and to investigate the role of Nesprin-1 in the pathogenesis of AD in a mouse model. METHODS: Blood and tissue specimens from AD patients were collected. The expression of Nesprin-1 in tissues from AD patients and non-AD patients with heart disease was studied by western blotting and quantitative real-time polymerase chain reaction (qRT-PCR). In addition, the expression and distribution of Nesprin-1 in AD and sham mice were compared in an induced AD mouse model, and detected by immunohistochemistry and qRT-PCR. RESULTS: Immunoblotting and qRT-PCR both showed that the expression of Nesprin-1 was significantly higher in AD versus control patients. An animal model of AD was established by continuous injection of Ang II into ApoE-/- mice. The expression of Nesprin-1 in aortic tissue of AD mice was higher than that of sham-operated mice as determined by immunohistochemistry. qRT-PCR showed that Nesprin-1 gene expression in aorta of AD mice was higher than that of sham-operated mice. CONCLUSIONS: An increased expression of Nesprin-1 was associated with AD, and hence Nesprin-1 may be involved in the pathogenesis of ADs. Preliminary findings suggest that Nesprin-1 may be a therapeutic target for the treatment of AD.