Background. Although the neutrophil percentage‐to‐albumin ratio (NPAR) has proven to be a robust systemic inflammation‐based predictor of mortality in a wide range of diseases, the prognostic value of the NPAR in critically ill patients with cardiogenic shock (CS) remains unknown. This study aimed at investigating the association between the admission NPAR and clinical outcomes in CS patients using real‐world data. Methods. Critically ill patients diagnosed with CS in the Medical Information Mart for Intensive Care‐III (MIMIC‐III) database were included in our study. The study endpoints included all‐cause in‐hospital, 30‐day, and 365‐day mortality in CS patients. First, the NPAR was analyzed as a continuous variable using restricted cubic spline Cox regression models. Second, X‐tile analysis was used to calculate the optimal cut‐off values for the NPAR and divide the cohort into three NPAR groups. Moreover, multivariable Cox regression analyses were used to assess the association of the NPAR groups with mortality. Results. A total of 891 patients hospitalized with CS were enrolled in this study. A nonlinear relationship between the NPAR and in‐hospital and 30‐day mortality was observed (all P values for nonlinear trend<0.001). According to the optimal cut‐off values by X‐tile, NPARs were divided into three groups: group I (NPAR < 25.3), group II (25.3 ≤ NPAR < 34.8), and group III (34.8 ≤ NPAR). Multivariable Cox analysis showed that higher NPAR was independently associated with increased risk of in‐hospital mortality (group III vs. group I: hazard ratio [HR] 2.60, 95% confidence interval [CI] 1.72‐3.92, P < 0.001), 30‐day mortality (group III vs. group I: HR 2.42, 95% CI 1.65‐3.54, P < 0.001), and 365‐day mortality (group III vs. group I: HR 6.80, 95% CI 4.10‐11.26, P < 0.001) in patients with CS. Conclusions. Admission NPAR was independently associated with in‐hospital, 30‐day, and 365‐day mortality in critically ill patients with CS.

Background: Acute myocardial infarction (AMI) is mainly caused by a mismatch of blood oxygen supply and demand in the myocardium. However, several studies have suggested that excessively high or low arterial oxygen tension could have deleterious effects on the prognosis of AMI patients. Therefore, the relationship between blood oxygenation and clinical outcomes among AMI patients is unclear, and could be nonlinear. In the critical care setting, blood oxygen level is commonly measured continuously using pulse oximetry-derived oxygen saturation (SpO₂). The present study aimed to determine the association between admission SpO₂ levels and all-cause in-hospital mortality, and to elucidate the optimal SpO₂ range with real-world data. Methods: Patients diagnosed with AMI on admission in the Medical Information Mart for Intensive Care III (MIMIC-III) database were included. A generalized additive model (GAM) with loess smoothing functions was used to determine and visualize the nonlinear relationship between admission SpO₂ levels within the first 24 hours after ICU admission and mortality. Moreover, the Cox regression model was constructed to confirm the association between SpO₂ and mortality. Results: We included 1,846 patients who fulfilled our inclusion criteria, among whom 587 (31.80%) died during hospitalization. The GAM showed that the relationship between admission SpO₂ levels and all-cause in-hospital mortality among AMI patients was nonlinear, as a U-shaped curve was observed. In addition, the lowest mortality was observed for an SpO₂ range of 94–96%. Adjusted multivariable Cox regression analysis confirmed that the admission SpO₂ level of 94–96% was independently associated with decreased mortality compared to SpO₂ levels 96% (HR 1.315; 95% CI: 1.018–1.658; P=0.030). Conclusions: The relationship between admission SpO₂ levels and all-cause in-hospital mortality followed a U-shaped curve among patients with AMI. The optimal oxygen saturation range was identified as an SpO₂ range of 94–96%, which was independently associated with increased survival in a large and heterogeneous cohort of AMI patients.

Background. Although serum calcium has been proven to be a predictor of mortality in a wide range of diseases, its prognostic value in critically ill patients with cardiogenic shock (CS) remains unknown. This retrospective observational study is aimed at investigating the association of admission calcium with mortality among CS patients. Methods. Critically ill patients diagnosed with CS in the Medical Information Mart for Intensive Care‐III (MIMIC‐III) database were included in our study. The study endpoints included 30‐day, 90‐day, and 365‐day all‐cause mortalities. First, admission serum ionized calcium (iCa) and total calcium (tCa) levels were analyzed as continuous variables using restricted cubic spline Cox regression models to evaluate the possible nonlinear relationship between serum calcium and mortality. Second, patients with CS were assigned to four groups according to the quartiles (Q1‐Q4) of serum iCa and tCa levels, respectively. In addition, multivariable Cox regression analyses were used to assess the independent association of the quartiles of iCa and tCa with clinical outcomes. Results. A total of 921 patients hospitalized with CS were enrolled in this study. A nonlinear relationship between serum calcium levels and 30‐day mortality was observed (all P values for nonlinear trend < 0.001). Furthermore, multivariable Cox analysis showed that compared with the reference quartile (Q3: 1.11 ≤ iCa < 1.17 mmol/L), the lowest serum iCa level quartile (Q1: iCa < 1.04 mmol/L) was independently associated with an increased risk of 30‐day mortality (Q1 vs. Q3: HR 1.35, 95% CI 1.00‐1.83, P = 0.049), 90‐day mortality (Q1 vs. Q3: HR 1.36, 95% CI 1.03‐1.80, P = 0.030), and 365‐day mortality (Q1 vs. Q3: HR 1.28, 95% CI 1.01‐1.67, P = 0.046) in patients with CS. Conclusions. Lower serum iCa levels on admission were potential predictors of an increased risk of mortality in critically ill patients with CS.

Background: The prognostic roles of three lymph node classifications, number of positive lymph nodes (NPLN), log odds of positive lymph nodes (LODDS), and lymph node ratio (LNR) in lung adenocarcinoma are unclear. We aim to find the classification with the strongest predictive power and combine it with the American Joint Committee on Cancer (AJCC) 8th TNM stage to establish an optimal prognostic nomogram. Methods: 25,005 patients with T1-4N0–2M0 lung adenocarcinoma after surgery between 2004 to 2016 from the Surveillance, Epidemiology, and End Results database were included. The study cohort was divided into training cohort (13,551 patients) and external validation cohort (11,454 patients) according to different geographic region. Univariate and multivariate Cox regression analyses were performed on the training cohort to evaluate the predictive performance of NPLN (Model 1), LODDS (Model 2), LNR (Model 3) or LODDS+LNR (Model 4) respectively for cancer-specific survival and overall survival. Likelihood-ratio χ² test, Akaike Information Criterion, Harrell concordance index, integrated discrimination improvement (IDI) and net reclassification improvement (NRI) were used to evaluate the predictive performance of the models. Nomograms were established according to the optimal models. They’re put into internal validation using bootstrapping technique and external validation using calibration curves. Nomograms were compared with AJCC 8th TNM stage using decision curve analysis. Results: NPLN, LODDS and LNR were independent prognostic factors for cancer-specific survival and overall survival. LODDS+LNR (Model 4) demonstrated the highest Likelihood-ratio χ² test, highest Harrell concordance index, and lowest Akaike Information Criterion, and IDI and NRI values suggested Model 4 had better prediction accuracy than other models. Internal and external validations showed that the nomograms combining TNM stage with LODDS+LNR were convincingly precise. Decision curve analysis suggested the nomograms performed better than AJCC 8th TNM stage in clinical practicability. Conclusions: We constructed online nomograms for cancer-specific survival and overall survival of lung adenocarcinoma patients after surgery, which may facilitate doctors to provide highly individualized therapy.

Aims: Molecular hydrogen has been exhibited a protective function in heart diseases. Our previous study demonstrated that hydrogen-rich saline (HRS) could scavenge free radicals selectively and alleviate the inflammatory response in the myocardial ischaemia/reperfusion (I/R) injury, but the underlying mechanism has not been fully clarified. Methods and results: Adult (10 weeks) C57BL/6 male mice and neonatal rat cardiomyocytes were used to establish I/R and hypoxia/reoxygenation (H/R) injury models. I/R and H/R models were treated with HRS to classify the mechanisms of cardioproctective function. In this study, we found that miR-124-3p was significantly decreased in both I/R and H/R models, while it was partially ameliorated by HRS pretreatment. HRS treatment also alleviated ischaemia-induced apoptotic cell death and increased cell viability during I/R process, whereas silencing expression of miR-124-3p abolished this protective effect. In addition, we identified calpain1 as a direct target of miR-124-3p, and up-regulation of miR-124-3 produced both activity and expression of calpain1. It was also found that compared with the HRS group, overexpression of calpain1 increased caspase-3 activities, promoted cleaved-caspase3 and Bax protein expressions, and correspondingly decreased Bcl-2, further reducing cell viability. These results illustrated that calpain1 overexpression attenuated protective effect of HRS on cardiomyocytes in H/R model. Conclusions: The present study showed a protective effect of HRS on I/R injury, which may be associated with miR-124-3p–calpain1 signalling pathway.

Background: The clinical efficiency of routine oxygen therapy is uncertain in patients with acute heart failure (AHF) who do not have hypoxemia. The aim of this study was to investigate the association between oxygen therapy and clinical outcomes in normoxemic patients hospitalized with AHF using real-world data. Methods: Normoxemic patients diagnosed with AHF on ICU admission from the electronic ICU (eICU) Collaborative Research Database were included in the current study, in which the study population was divided into the oxygen therapy group and the ambient-air group. Propensity score matching (PSM) was applied to create a balanced covariate distribution between patients receiving supplemental oxygen and those exposed to ambient air. Linear regression and logistic regression models were performed to assess the associations between oxygen therapy and length of stay (LOS), and all-cause in-hospital as well as ICU mortality rates, respectively. A series of sensitivity and subgroup analyses were conducted to further validate the robustness of our findings. Results: A total of 2922 normoxemic patients with AHF were finally included in the analysis. Overall, 42.1% (1230/2922) patients were exposed to oxygen therapy, and 57.9% (1692/2922) patients did not receive oxygen therapy (defined as the ambient-air group). After PSM analysis, 1122 pairs of patients were matched: each patient receiving oxygen therapy was matched with a patient without receiving supplemental oxygen. The multivariable logistic model showed that there was no significant interaction between the ambient air and oxygen group for all-cause in-hospital mortality [odds ratio ( OR ) 1.30; 95% confidence interval (CI) 0.92–1.82; P = 0.138] or ICU mortality ( OR 1.39; 95% CI 0.83–2.32; P = 0.206) in the post-PSM cohorts. In addition, linear regression analysis revealed that oxygen therapy was associated with prolonged ICU LOS ( OR 1.11; 95% CI 1.06–1.15; P < 0.001) and hospital LOS ( OR 1.06; 95% CI 1.01–1.10; P = 0.009) after PSM. Furthermore, the absence of an effect of supplemental oxygen on mortality was consistent in all subgroups. Conclusion: Routine use of supplemental oxygen in AHF patients without hypoxemia was not found to reduce all-cause in-hospital mortality or ICU mortality.