Background: Oxygen therapy with high-flow nasal cannula (HFNC) is being increasingly used in patients with acute heart failure (AHF), but its impact on short-term outcomes has been poorly reported. This study aims to compare short-term outcomes in patients with AHF and respiratory distress who received initial oxygen therapy with HFNC versus noninvasive ventilation (NIV) in the emergency department (ED).
Methods: In this retrospective analysis of prospectively collected data from a multicenter registry, we included all patients diagnosed with AHF in 35 Spanish EDs during January–February 2022 who received either HFNC or NIV as initial oxygen therapy. Patient allocation to initial HFNC or NIV was left to the discretion of the treating emergency physician. The primary outcome was 30-day all-cause mortality. Secondary outcomes included treatment failure (defined as the need for switch of oxygen therapy techniques or escalation to NIV to mechanical ventilation), intensive care unit admission, endotracheal intubation, in-hospital mortality, a composite endpoint of intubation or 7-day mortality, and prolonged hospitalization (>7 days). Associations were expressed as adjusted odds ratios (aOR) with 95% confidence intervals (CIs), using age, sex, and significant patient-and episode-related characteristics as covariates.
Results: Of 4301 patients with AHF, 330 (7.7%) were included (median age: 83 years; 57% women): 71 received HFNC and 259 received NIV. No statistically significant between-group differences were detected in the measured baseline characteristics; however, residual imbalance and unmeasured confounding cannot be excluded. A total of 66 (20.1%) patients died during 30-day follow-up with no significant difference between HFNC (21.4%) and NIV (19.8%) groups (aOR: 1.09; 95% CI: 0.55–2.17). HFNC was more frequently followed by a change or escalation in respiratory support (23.9% vs. 2.3%, aOR: 17.9; 95% CI: 5.90–54.2). This composite outcome was mainly driven by switches from HFNC to NIV (13/17 cases in the HFNC group) rather than by escalation to invasive mechanical ventilation, and should not be interpreted as direct evidence that HFNC was clinically inferior to NIV. But no significant differences were found for the other secondary endpoints.
Conclusion: In this analysis of patients with AHF treated in the ED, no statistically significant between-group difference in 30-day mortality was detected between initial HFNC and NIV. However, given the wide confidence intervals, these findings do not establish equivalence. Larger randomized trials are warranted to confirm the comparative effectiveness of these two oxygenation strategies.

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: Since it remains unclear whether Shen-fu injection (SFI) could be used in hemorrhagic shock (HS), this study aimed to explore the effects of SFI on lung injury caused by HS in a porcine model.
Methods: After HS induction, 32 pigs were allocated using simple randomization to four groups (n = 8 each): Group I (no resuscitation), Group II (shed blood reinfusion), Group III (reinfusion + saline 3 mL/kg), and Group IV (reinfusion + Shenfu injection 3 mL/kg). At 6 hours after HS, lung tissue was collected to measure IL‑6, IL‑8, IL‑4, and IL‑10 by ELISA, and to evaluate apoptosis by immunohistochemistry and transmission electron microscopy. Tissues from non‑survivors were obtained at the time of death and analyzed when available.
Results: Of the 32 randomized animals, 23 survived to 6 hours (Group I, 4/8; Group II, 6/8; Group III, 6/8; Group IV, 7/8). Cytokine analysis revealed that group IV exhibited significantly reduced levels of proinflammatory cytokines, including IL-6 and IL-8, concomitant with elevated concentrations of anti-inflammatory cytokines, specifically IL-4 and IL-10 (P < 0.05). Additionally, group IV demonstrated significantly elevated superoxide dismutase enzymatic activity, alongside enhanced Na⁺-K⁺-ATPase and Ca²⁺-ATPase activities, coupled with markedly reduced malondialdehyde levels (P < 0.05). Immunohistochemical analysis revealed downregulated caspase-3 expression and upregulated Bcl-2 expression in group IV, collectively indicating attenuated apoptotic activity. Ultrastructural examination of pulmonary tissues further demonstrated that SFI administration effectively ameliorated alveolar edema, hemorrhage, and inflammatory cell infiltration, while concurrently mitigating epithelial cell apoptosis and mitochondrial injury relative to the other experimental groups.
Conclusion: Among animals surviving to the 6‑hour assessment, SFI was associated with differences in selected inflammatory, oxidative‑stress, apoptosis, and histological markers. Because of differential mortality, small outcome‑specific sample sizes, and limited quantitative histology, these findings should be considered exploratory and do not establish improved survival or hemodynamic benefit.

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.

Stroke, a devastating neurological disorder resulting from acute cerebrovascular injury, represents the second most common cause of global mortality and a predominant contributor to long-term disability. Aldehyde dehydrogenase 2 (ALDH2) is a critical mitochondrial enzyme that plays a pivotal role in the metabolism of toxic reactive aldehydes, including 4-hydroxynonenal and acetaldehyde. The rs671 (Glu504Lys) polymorphism of ALDH2, which exhibits remarkably high prevalence in East Asian populations, has emerged as a genetic determinant of stroke susceptibility and recovery. This narrative review provides an overview of the multifaceted relationship between ALDH2 genetic variants and stroke. We summarize the reported associations of ALDH2 polymorphisms with stroke incidence and clinical outcomes, describe the neuroprotective mechanisms mediated by ALDH2 enzymatic activity, and discuss the dual role of ALDH2 in Mendelian randomization studies-as an instrumental variable in alcohol-related research and as a mediator of cerebrovascular risk with potential therapeutic relevance. Throughout, we emphasize the areas of uncertainty and the conflicting findings that remain in this field. By integrating epidemiological findings with mechanistic insights, this review offers a translational perspective on ALDH2 as a potential biomarker and a candidate target for stroke prevention and management.

The excess accumulation of fluid in the extracellular space of the heart determines a condition of “myocardial interstitial edema.” Myocardial edema is present in multiple pathological conditions observed in the intensive care setting: fulminant myocarditis, sepsis-induced cardiomyopathy, cardiac arrest, capillary leak syndrome, and extracorporeal circulation. Fluid accumulation in the interstitium can occur rapidly, leading to severe heart failure and potentially progressing to cardiogenic shock. Early diagnosis and prompt therapy are crucial. Understanding the factors and diseases that can disrupt myocardial fluid homeostasis and contribute to the development of interstitial edema allows for a targeted therapeutic approach, aimed at reducing fluid accumulation and clinical detrimental effects.

Background: Continuous renal replacement therapy (CRRT) is commonly used to manage sepsis-associated acute kidney injury (SA-AKI) as a form of extracorporeal blood purification. However, the current consensus report from the 28th Acute Disease Quality Initiative workgroup does not provide explicit recommendations for the use of CRRT in SA-AKI, because of insufficient high-quality evidence regarding its efficacy. This study aimed to evaluate whether CRRT provides clinical benefits compared with non-CRRT therapy in patients with SA-AKI.
Methods: All randomized controlled trials published up to October 11, 2025, in 9 Chinese and English databases were reviewed and included in the study. A meta-analysis was performed on the experimental group (CRRT group) and control group (non-CRRT group) using risk ratios (RRs), weighted mean differences (WMDs), and 95% confidence intervals (CIs). The certainty of evidence for each outcome was evaluated using the Grading of Recommendations Assessment, Development and Evaluation approach.
Results: A total of 37 studies involving 3120 subjects were included. Compared with the non-CRRT group, CRRT was associated with reduced 28-day mortality (RR: 0.46, 95% CI: 0.34–0.61, P < 0.01), hospital mortality (RR: 0.39, 95% CI: 0.28–0.54, P < 0.01), and incidence of cardiovascular events (RR: 0.39, 95% CI: 0.28–0.55, P < 0.01). CRRT was also associated with shorter intensive care unit length of stay (WMD: -3.97, 95% CI: -4.71 to -3.22, P < 0.01) and in-hospital length of stay (WMD: -4.51, 95% CI: -5.51 to -3.51, P < 0.01).
Conclusion: The pooled estimates from the included studies favored CRRT with respect to 28-day mortality, hospital mortality, incidence of cardiovascular events, ICU length of stay, and in-hospital length of stay; however, the certainty of evidence was low to very low because of methodological limitations, heterogeneity in CRRT definitions and treatment protocols, small study sizes, and limited geographic generalizability. These findings should not be interpreted as establishing a routine clinical benefit of CRRT in SA-AKI or as supporting CRRT initiation in patients without standard indications for kidney replacement therapy. Further independent, prospectively registered, multicenter randomized controlled trials with standardized CRRT protocols are needed to confirm these findings.

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.