Background: We performed an exploratory secondary analysis of a public transcriptomic dataset to identify gene-expression patterns associated with 7-day outcome among 14 patients receiving ECMO for cardiogenic shock after acute myocardial infarction. Methods: The microarray dataset (GSE93101, n = 14) was retrieved from the Gene Expression Omnibus online database. Differential expression, weighted gene co-expression network analyses (WGCNA), Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed. To identify the top five hub genes, we used the mutual construction of the protein–protein interaction network and the Cytoscape software. Subsequently, a gene–microRNA (miRNA) network was established to identify the miRNAs that potentially regulate these hub genes. Results: Ten genes were obtained when those in the two highest correlation modules of WGCNA were intersected with the differentially expressed genes. A total of 104 differentially expressed genes were found to be associated with oxidoreductase activity and metabolic pathways. We found the top five hub genes using the Cytoscape software: CD68, C8A, NR1H4, and ADGRE1 genes were downregulated, while TMPRSS6 was upregulated. TMPRSS6 had the highest degree of affinity and was regulated by 29 miRNAs, while CD68, NR1H4, CD163, and C8A were regulated by 18, 14, 14, and 2 miRNAs, respectively. Although CD163 was not in the top five hub genes, it is regulated by more miRNAs. Conclusion: Through comprehensive analysis, CD68, which was regulated by 18 miRNAs, emerged as a promising prognostic biomarker for ECMO after AMI, and the mechanism may reflect macrophage activation and differentiation, thereby modulating postinfarction inflammatory responses and tissue repair.
Background: Large, mobile left atrial thrombi can intermittently occlude the mitral orifice and precipitate rapid hemodynamic compromise in atrial fibrillation. Timely echocardiography is pivotal to diagnosis and management. Case presentation: A 71-year-old woman with previously undocumented atrial fibrillation presented with dyspnea, rapid ventricular response, and borderline blood pressure (100/50 mmHg). Transthoracic echocardiography showed a large, mobile left atrial mass prolapsing through the mitral valve; transesophageal echocardiography confirmed a 3.3 × 2.8 cm thrombus with spontaneous echo contrast and 2 smaller septal thrombi. Mitral leaflets were thickened and calcified with commissural fusion, consistent with rheumatic disease; the transmitral gradient was mild, but biatrial enlargement suggested chronic pathology. Given thrombus size and mobility, anticoagulation and thrombolysis were deferred. The patient underwent emergency surgical thrombectomy, bioprosthetic mitral valve replacement, and left atrial appendage exclusion. Recovery was uneventful, with normal prosthetic function and no residual thrombus on follow-up imaging. Conclusion: In atrial fibrillation with suspected mechanical obstruction, bedside transthoracic echocardiography followed by transesophageal echocardiography enables rapid confirmation of a ball-valve left atrial thrombus. In this patient, rapid echocardiographic characterization and multidisciplinary assessment supported urgent surgery because of intermittent mechanical obstruction, marked thrombus mobility, associated mitral-valve disease, and the need for definitive treatment. Management should be individualized; this single case does not establish the superiority of surgery over anticoagulation for all large left atrial thrombi.
Background: Bronchopulmonary dysplasia (BPD) is a complex chronic lung disease caused by the interaction between lung development and prenatal and postnatal injury events. Up to one-third of infants with BPD further develop pulmonary vascular dysfunction, leading to chronic pulmonary hypertension (PH). Infants with BPD-PH face increased mortality, a higher risk of adverse neurodevelopmental outcomes, and a lack of effective treatments. Methods: A total of 30 study participants were recruited from the Children’s Hospital Affiliated to Shandong University, with the data collection period spanning from January 2023 to May 2025. Through metabolite analysis, we observed serum arginine concentrations were lower in the BPD-PH group than in the comparison group, but the between-group difference did not reach statistical significance (P = 0.0581). Subsequently, in vitro experiments were conducted to investigate the effects of arginine on the proliferation and migration abilities of vascular endothelial cells and to elucidate the underlying molecular mechanisms. Finally, in vivo experiments were performed to validate the protective role of arginine in BPD-PH. Results: The results of the in vitro experiments indicate that arginine inhibits the proliferation and migration of vascular endothelial cells. Molecular mechanism studies revealed that arginine reduces the expression of α-smooth muscle actin, hypoxia-inducible factor-1α, and related proteins through the arginyl-tRNA synthetase-1 (RARS1)-hairy and enhancer of split homologue-1 (HES1) pathway, RARS1 and HES1 were detected in the same immunoprecipitated protein complex, supporting a possible involvement of RARS1–HES1 signaling. In neonatal rats exposed to hyperoxia, arginine supplementation was associated with changes in selected lung-tissue mRNA markers. Pulmonary hemodynamics, right-ventricular remodeling, vascular morphometry, and alveolar structure were not assessed. Conclusion: Our results indicate that arginine alleviates BPD-PH by promoting vascular endothelial cell remodeling through the RARS1-HES1 pathway. Arginine supplementation may represent a novel therapeutic alternative for preventing BPD.
Background: Endotracheal intubation of critically ill patients is associated with various complications, mainly hypotension. The administration of an intravenous fluid bolus before induction of anesthesia has been used to prevent hypotension during endotracheal intubation in the intensive care unit (ICU). However, some patients still experience hemodynamic instability. Therefore, this study was conducted to compare the effect of a fluid bolus alone and a fluid bolus plus low-dose noradrenaline infusion on cardiovascular collapse among critically ill adults before tracheal intubation. Methods: The randomized trial enrolled 136 critically ill patients who required endotracheal intubation. Patients were allocated to the intravenous fluid (group A) and the intravenous fluid plus low-dose noradrenaline group (group B). Cardiovascular collapse, hypotension, and other secondary outcomes were recorded. Results: Vasopressor requirement at 2 minutes postinduction was lower in group B (39.7%) than in group A (44.1%). Cardiac arrest within 1 hour occurred in 2.9% of patients in group A. Death within 1 hour occurred in 2.9% patients of group A and 1.5% of group B. The requirement for renal replacement therapy, duration of vasopressor requirement and inhospital mortality were higher in group B. The duration of ICU stay and the duration of ventilator requirement were higher in group A. All these differences were statistically insignificant except for the total duration of hospital stay, which was longer in group A than in group B ( P = 0.036). Conclusion: Among critically ill patients undergoing tracheal intubation, the administration of intravenous fluid bolus plus low-dose noradrenaline, compared with a fluid bolus alone, did not significantly reduce the incidence of cardiovascular collapse.
