Background Ischemic cardiomyopathy (ICM) is one of the most usual causes of death worldwide. This study aimed to find the candidate gene for ICM. Methods We studied differentially expressed genes (DEGs) in ICM compared to healthy control. According to these DEGs, we carried out the functional annotation, protein-protein interaction (PPI) network and transcriptional regulatory network constructions. The expression of selected candidate genes were confirmed using a published dataset and Quantitative real time polymerase chain reaction (qRT-PCR). Results From three Gene Expression Omnibus (GEO) datasets, we acquired 1081 DEGs (578 up-regulated and 503 down-regulated genes) between ICM and healthy control. The functional annotation analysis revealed that cardiac muscle contraction, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and dilated cardiomyopathy were significantly enriched pathways in ICM. SNRPB, BLM, RRS1, CDK2, BCL6, BCL2L1, FKBP5, IPO7, TUBB4B and ATP1A1 were considered the hub proteins. PALLD, THBS4, ATP1A1, NFASC, FKBP5, ECM2 and BCL2L1 were top six transcription factors (TFs) with the most downstream genes. The expression of 6 DEGs (MYH6, THBS4, BCL6, BLM, IPO7 and SERPINA3) were consistent with our integration analysis and GSE116250 validation results. Conclusions The candidate DEGs and TFs may be related to the ICM process. This study provided novel perspective for understanding mechanism and exploiting new therapeutic means for ICM.
Background It’s necessary to analyze the related risk factors and complications of low cardiac output syndrome (LCOS) after operation in children with congenital heart disease (CHD), to elucidate the management strategy of LCOS. Methods CHD children admitted to the department of cardiology in our hospital from January 15, 2019 to October 31, 2020 were included. The personal and clinical data of CHD children with LCOS and without LCOS were collected and compared. Logistic regression analyses were conducted to identify the risk factors of postoperative LCOS. Besides, the complication and mortality of LCOS and no LCOS patients were compared. Results A total of 283 CHD patients were included, the incidence of postoperative LCOS in CHD patients was 12.37%. There were significant differences in the age, preoperative oxygen saturation, two-way ventricular shunt, duration of CPB and postoperative residual shunt between two groups (all p < 0.05). Logistic regression analyses indicated that age ≤ 4y(OR2.426, 95%CI1.044 ~ 4.149), preoperative oxygen saturation ≤ 93%(OR2.175, 95%CI1.182 ~ 5.033), two-way ventricular shunt (OR3.994, 95%CI1.247 ~ 6.797), duration of CPB ≥ 60 min(OR2.172, 95%CI1.002 ~ 4.309), postoperative residual shunt (OR1.487, 95%CI1.093 ~ 2.383) were the independent risk factors of LCOS in patients with CHD (all p < 0.05). There were significant differences in the acute liver injury, acute kidney injury, pulmonary infection, tracheotomy, duration of mechanical ventilation, length of ICU stay and mortality (all p < 0.05), no significant difference in the 24 h drainage was found(p = 0.095). Conclusion LCOS after CHD is common, more attentions should be paid to those patients with age ≤ 4y, preoperative oxygen saturation ≤ 93%, two-way ventricular shunt, duration of CPB ≥ 60 min, postoperative residual shunt to improve the prognosis of CHD patients.
Statins exert pleiotropic effects on endothelial cells, in addition to lowering cholesterol. This study evaluated angiotensin II (Ang II)-induced dysfunction in human umbilical vein endothelial cells (HUVECs), and the effects of atorvastatin (Ator) on induced HUVECs in vitro. The cytotoxicity of Ang II and Ator was determined by the MTT assay. A series of cellular responses were screened, including oxidative stress, cellular apoptosis, inflammatory response, autophagy, expression of endothelial nitric oxide synthase and the angiogenic function of HUVECs. Ator returned these cellular responses to a normal level. The present study also examined cellular organelle dysfunction. In HUVECs, Ang II triggered mitochondrial damage, as demonstrated by a decreased mitochondrial membrane potential, while Ator attenuated this Ang II-induced damage. The observed cellular dysfunction may cause endothelial senescence due to excessive cell injury. The current study examined several aging markers, which revealed that these disorders of cellular functions triggered endothelial senescence, which was delayed by Ator. Ator also suppressed Ang II-induced angiogenesis damage. The data presented in this study strongly suggested that Ang II induced a series of processes that lead to cellular dysfunction in HUVECs, including oxidative stress, inflammation, and mitochondrial damage, leading to apoptosis and endothelial senescence. However, Ator significantly reversed these effects and modulated intracellular stability. The present study indicated that Ator serves an antagonistic role against HUVEC dysfunction and may potentially prevent several diseases, including coronary disease and atherosclerosis, by maintaining cellular homeostasis.
Background and Aims: Patients with heart failure with reduced ejection fraction (HFrEF) are among the most challenging patients undergoing coronary artery bypass grafting surgery (CABG). Several surgical risk scores are commonly used to predict the risk in patients undergoing CABG. However, these risk scores do not specifically target HFrEF patients. We aim to develop and validate a new nomogram score to predict the risk of in-hospital mortality among HFrEF patients after CABG.Methods: The study retrospectively enrolled 489 patients who had HFrEF and underwent CABG. The outcome was postoperative in-hospital death. About 70% (n = 342) of the patients were randomly constituted a training cohort and the rest (n = 147) made a validation cohort. A multivariable logistic regression model was derived from the training cohort and presented as a nomogram to predict postoperative mortality in patients with HFrEF. The model performance was assessed in terms of discrimination and calibration. Besides, we compared the model with EuroSCORE-2 in terms of discrimination and calibration.Results: Postoperative death occurred in 26 (7.6%) out of 342 patients in the training cohort, and in 10 (6.8%) out of 147 patients in the validation cohort. Eight preoperative factors were associated with postoperative death, including age, critical state, recent myocardial infarction, stroke, left ventricular ejection fraction (LVEF) ≤35%, LV dilatation, increased serum creatinine, and combined surgery. The nomogram achieved good discrimination with C-indexes of 0.889 (95%CI, 0.839–0.938) and 0.899 (95%CI, 0.835–0.963) in predicting the risk of mortality after CABG in the training and validation cohorts, respectively, and showed well-fitted calibration curves in the patients whose predicted mortality probabilities were below 40%. Compared with EuroSCORE-2, the nomogram had significantly higher C-indexes in the training cohort (0.889 vs. 0.762, p = 0.005) as well as the validation cohort (0.899 vs. 0.816, p = 0.039). Besides, the nomogram had better calibration and reclassification than EuroSCORE-2 both in the training and validation cohort. The EuroSCORE-2 underestimated postoperative mortality risk, especially in high-risk patients.Conclusions: The nomogram provides an optimal preoperative estimation of mortality risk after CABG in patients with HFrEF and has the potential to facilitate identifying HFrEF patients at high risk of in-hospital mortality.
Background: Hypertrophic cardiomyopathy (HCM) is the most common chromosomal abnormal heart disease. The pathophysiological mechanism of HCM is complex. Several studies have suggested that the level of Soluble ST2 (sST2) may be a biomarker of chronic systolic heart failure, however, the role of sST2 in HCM remains unclear. So we performed this study to analyze the role of Soluble ST2 (sST2), and its correlations with clinical prognosis of patients with hypertrophic cardiomyopathy (HCM) undergoing ventricular septal myectomy.Methods: HCM patients who underwent modified Morrow surgery in our hospital during June 2016-June 2018 were included. We divided the patients into different groups stratified by sST2 and Gal-3 level. Besides, we included volunteers without heart disease for medical examination as normal controls. Biochemical analyses were conducted to identify the biomarkers difference. The predictive value of sST2 and Gal-3 on all-cause mortality was evaluated with Cox regression analysis.Results: A total of 125 HCM patients were included in this present study. The sST2 and Gal-3 levels in HCM patients were significantly higher than that in control group (all P<0.001); there were significant differences in the incidence of all-cause mortality for HCM patients stratified by the sST2 and Gal-3 level;
BackgroundQuantitative flow ratio (QFR) is a new functional index to assess the functional significance of coronary stenosis. While whether there is an association between QFR and transit-time flow measurement (TTFM) parameters of the target coronary artery has not been well addressed.MethodsA total of 89 patients receiving the in situ left internal thoracic artery (LITA) grafts to the left anterior descending artery (LAD), and 19 patients undergoing the saphenous vein grafts (SVG) were enrolled in this retrospective study. The QFR value of the LAD was evaluated preoperatively. According to the QFR values, patients with the LITA to the LAD bypass grafts were divided into two groups (group A1: QFR < 0.75, group A2: QFR ≥ 0.75), and SVG patients were divided into two groups (V1 group: QFR < 0.75, V2 group: QFR ≥ 0.75).ResultsIn groups A1 and A2, respectively, median graft flow (Qm) was 44 (34) mL/minute and 26.5 (30.0) ml/minute; median pulsatility index (PI) was 2.00 (1.00) and 2.65 (0.90). Significant differences were observed in Qm (P = 0.034) and PI (P = 0.030). And the correlation coefficients of the TTFM variables with QFR were Qm: r = r = −0.226, (P = 0.036), PI: r = 0.265 (P = 0.012) among the LITA to LAD population.ConclusionTTFM variables, especially the PI, of the LITA in situ graft to the LAD during Coronary artery bypass grafting (CABG) are strongly affected by preoperative QFR values. Moreover, in functionally mild coronary stenosis, the chance of competitive flow increases.
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