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Background: The timing of central venous pressure (CVP) measurement may play a crucial role in heart failure management, yet no studies have explored this aspect. Methods: Clinical information pertaining to patients in critical condition with a diagnosis of heart failure was retrieved from the MIMIC-IV database. The association between initial measurements of central venous pressure (CVP) and the incidence of mortality from all causes was analyzed using the Cox proportional hazards approach. Subgroup analysis and propensity score matching were conducted for sensitivity analyses. Results: This study included 11,241 participants (median age, 75 years; 44.70 % female). Utilizing restricted cubic spline and Kaplan–Meier survival analyses, it was determined that prognostic outcomes were better when CVP was measured within the initial 5-h window. Multivariate-adjusted 1-year (HR: 0.69; 95 % CI: 0.61–0.77), 90-day (HR: 0.70; 95 % CI: 0.62–0.80), and 30-day (HR: 0.67; 95 % CI: 0.57–0.78) all-cause mortalities were significantly lower in patients with early CVP measurement, which was proved robustly in subgroup analysis. Subsequent to the application of propensity score matching, a cohort of 1536 matched pairs was established, with the observed mortality rates continuing to be significantly lower among participants who underwent early CVP assessment. Conclusions: Early CVP measurement (within 5 h) demonstrated an independent correlation with a decrease in both immediate and extended all-cause mortality rates among patients in critical condition suffering from heart failure.

Background: Pulmonary arterial hypertension (PAH) represents a substantial global risk to human health. This study aims to identify diagnostic biomarkers for PAH and assess their association with the immune microenvironment through the utilization of sophisticated bioinformatics techniques. Methods: Based on two microarray datasets, differentially expressed genes (DEGs) were detected, and hub genes underwent a sequence of machine learning analyses. After pathways associated with PAH were assessed by gene enrichment analysis, the identified genes were validated using external datasets and confirmed in a monocrotaline (MCT)-induced rat model. In addition, three algorithms were employed to estimate the proportions of various immune cell types, and the link between hub genes and immune cells was substantiated. Results: Using SVM, LASSO, and WGCNA, we identified seven hub genes, including (BPIFA1, HBA2, HBB, LOC441081, PI15, S100A9, and WIF1), of which only BPIFA1 remained stable in the external datasets and was validated in an MCT-induced rat model. Furthermore, the results of the functional enrichment analysis established a link between PAH and both metabolism and the immune system. Correlation assessment showed that BPIFA1 expression in the MCP-counter algorithm was negatively associated with various immune cell types, positively correlated with macrophages in the ssGSEA algorithm, and correlated with M1 and M2 macrophages in the CIBERSORT algorithm. Conclusion: BPIFA1 serves as a modulator of PAH, with the potential to impact the immune microenvironment and disease progression, possibly through its regulatory influence on both M1 and M2 macrophages.