Positive association between sodium-to-chloride ratio and in-hospital mortality of acute heart failure.

Previous studies have suggested that levels of sodium and chloride in the blood may be indicative of the prognosis of different medical conditions. Nevertheless, the assessment of the prognostic significance of the sodium-to-chloride (Na/Cl) ratio in relation to in-hospital mortality among individuals suffering from acute heart failure (AHF) remains unexplored. In this study, the participants were selected from the Medical Information Mart for Intensive Care IV database and divided into three groups based on the Na/Cl ratio level upon admission. The primary results were the mortality rate within the hospital. Cox regression, Kaplan-Meier curves, receiver operator characteristic (ROC) curve analysis and subgroup analyses were utilized to investigate the correlation between the admission Na/Cl ratio and outcomes in critically ill patients with AHF. A total of 7844 patients who met the selection criteria were included in this study. After adjusting for confounders, the multivariable Cox regression analysis revealed that the baseline Na/Cl ratio significantly elevated the risk of in-hospital mortality among critically ill patients with AHF (HR = 1.34, 95% CI 1.21-1.49). Furthermore, when the Na/Cl ratio was converted into a categorical factor and the initial tertile was taken as a point of comparison, the hazard ratios (HRs) and 95% confidence intervals (CIs) for the second and third tertiles were 1.27 (1.05-1.54) and 1.53 (1.27-1.84), respectively. Additionally, a P value indicating a significant trend of < 0.001 was observed. ROC curve analysis showed that Na/Cl ratio had a more sensitive prognostic value in predicting in-hospital mortality of AHF than the sodium or chloride level alone (0.564 vs. 0.505, 0.544). Subgroup examinations indicated that the association between the Na/Cl ratio upon admission and the mortality rate of critically ill patients with AHF remained consistent in the subgroups of hyponatremia and hypochlorhydria (P for interaction > 0.05). The linear relationship between the Na/Cl ratio and in-hospital mortality in AHF patients indicates a positive association.

Comparison of the effects of using feedback devices for training or simulated cardiopulmonary arrest.

BACKGROUND: High-quality chest compression is essential for successful cardiac arrest resuscitation. High-quality cardiopulmonary resuscitation (CPR) can effectively improve the survival rate of patients with cardiopulmonary arrest. However, bystanders untrained in cardiopulmonary resuscitation may provide inadequate chest compressions. Previous studies have shown that the use of feedback devices in training alone or in simulated cardiopulmonary arrest alone can improve cardiopulmonary resuscitation. This study aims to determine whether using an audiovisual feedback (AVF) device during CPR training or a simulated cardiopulmonary arrest (CA) scenario would be more effective in improving the quality of chest compressions (CC). METHODS: We use a prospective, randomized, 2 × 2 factorial design trial. A total of 160 participants from Wuhan University and senior clinical medicine undergraduates who had not participated in any CPR training before and had no actual CPR experience are recruited. Each participant is randomized to 1 of 4 permutations, including AVF device vs. no AVF device during CPR training and AVF device vs. no AVF device during simulated CA. Main outcomes and measures are the depth, the percentage of CCs with correct depth (5-6 cm), the rate of CCs, and the percentage of CCs with the correct rate (100-120 cpm). RESULTS: The use of the AVF device during simulated CA resulted in improved CC quality. In CA without AVF device, the average compression depth and the percentage of adequate depth with AVF device are 5.1 cm, 5.0 cm and 55.5%, 56.3%, respectively, which are higher than those without AVF device (4.5 cm, 4.7 cm and 32.8%, 33.6%). (p = 0.011, p = 0.000, both < 0.05).Compared with CA without AVF device, the average compression rate and the percentage of adequate rate with AVF device are 112.3 cpm, 111.2 cpm and 79.4%, 83.1%, respectively. The average compression rate and the percentage of adequate rate without using the AVF device are 112.4 cpm, 110.3 cpm and 71.5%, 68.5%, respectively. (p = 0.567 > 0.05, p = 0.017 < 0.05)Although the average compression rate in group D is slightly lower than that in group C, the percentage of suitable frequency with the feedback device is still higher than that without AVF device. CONCLUSION: Using a feedback device during simulated cardiopulmonary arrest is more effective in improving cardiopulmonary resuscitation than during training.

Construction of LncRNA-mediated CeRNA network for investigating the immune pathogenesis of myocardial infarction.

BACKGROUND: Myocardial infarction (MI) is a cardiovascular disease that seriously threatens human health. However, an immune-related competitive endogenous RNA (ceRNA) network has not been reported in MI. METHODS: The GSE66360, GSE19339, GSE97320, GSE61741, and GSE168281 datasets were acquired from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) and differentially expressed miRNAs (DEmiRNAs) from MI patients and healthy controls were screened and an immune-related ceRNA network was constructed. Furthermore, the key long noncoding RNAs(lncRNAs) highly related to the immune mechanism of MI were identified utilizing the random walk with restart algorithm. Finally, the expression of the hub genes was further verified in the GSE66360, GSE19339, and GSE97320 datasets, and quantitativereal-time polymerase chain reaction (qRT-PCR) was performed for the MI patients and healthy controls. RESULTS: A total of 184 differentially expressed immune-related genes(DE-IRGs) and 432 DE-miRNAs were obtained, and an immune-related ceRNA network comprising 1421 lncRNAs, 61 DE-miRNAs, and 139 DE-IRGs was constructed. According to the order of stress, betweenness, and closeness, NEAT1, KCNQ1OT1, and XIST were identified as key lncRNAs. Moreover, random walk with restart analysis also suggested that NEAT1, KCNQ1OT1, and XIST are key lncRNAs. Subsequently, a ceRNA network of 10 hub genes and 3 lncRNAs was constructed. Finally, we found that the expression of FCER1G and TYROBP significantly differed between MI patients and control individuals in the GSE66360, GSE19339, and GSE97320 datasets. qRT-PCR revealed that the expression of NEAT1, KCNQ1OT1, XIST, FCER1G, and TYROBP was significantly elevated in MI tissue samples compared to healthy control tissue samples. CONCLUSION: NEAT1, KCNQ1OT1, XIST, FCER1G, and TYROBP are involved in MI and can be used as molecular biomarkers for the screening and diagnosis of MI. Furthermore, the immune system plays an essential role in the onset and progression of MI.

Age­adjusted Charlson comorbidity index and in­hospital mortality in critically ill patients with cardiogenic shock: A retrospective cohort study.

Evidence regarding the relationship between age-adjusted Charlson comorbidity index (ACCI) and in-hospital mortality is limited. Therefore, the present study investigated whether there was an independent association between ACCI and in-hospital mortality in critically ill patients with cardiogenic shock (CS) after adjusting for other covariates (age, sex, history of disease, scoring system, in-hospital management, vital signs at presentation, laboratory findings and vasopressors). ACCI, calculated retrospectively after hospitalization between 2008 and 2019, was derived from intensive care unit (ICU) admissions at the Beth Israel Deaconess Medical Center (Boston, MA, USA). Patients with CS were classified into two categories based on predefined ACCI scores (low, <8; high, ≥8). Based on baseline ACCI, the risk of in-hospital mortality in patients with CS was calculated using a multivariate Cox proportional risk model, and the threshold effect was calculated using a two-piece linear regression model. The in-hospital mortality rate was ~1.5 times greater in the ACCI high group compared with that in the ACCI low group [hazard ratio (HR)=1.45; 95% confidence interval (CI), 1.14-1.86]. Additional analysis showed that ACCI had a curvilinear association with in-hospital mortality risk in patients with CS, with a saturation effect predicted at 4.5. When ACCI was >4.5, the risk of in-hospital CS death increased significantly with increasing ACCI (HR=1.122; 95% CI, 1.054-1.194). Overall, ACCI was an independent predictor of in-hospital mortality in ICU patients with CS. A non-linear relationship was revealed between ACCI and in-hospital mortality, where in-hospital mortality increased significantly when ACCI was >4.5.

The Charlson comorbidity index and short-term readmission in patients with heart failure: A retrospective cohort study.

The relationship between the Charlson comorbidity index (CCI) and short-term readmission is as yet unknown. Therefore, we aimed to investigate whether the CCI was independently related to short-term readmission in patients with heart failure (HF) after adjusting for other covariates. From December 2016 to June 2019, 2008 patients who underwent HF were enrolled in the study to determine the relationship between CCI and short-term readmission. Patients with HF were divided into 2 categories based on the predefined CCI (low < 3 and high > =3). The relationships between CCI and short-term readmission were analyzed in multivariable logistic regression models and a 2-piece linear regression model. In the high CCI group, the risk of short-term readmission was higher than that in the low CCI group. A curvilinear association was found between CCI and short-term readmission, with a saturation effect predicted at 2.97. In patients with HF who had CCI scores above 2.97, the risk of short-term readmission increased significantly (OR, 2.66; 95% confidence interval, 1.566-4.537). A high CCI was associated with increased short-term readmission in patients with HF, indicating that the CCI could be useful in estimating the readmission rate and has significant predictive value for clinical outcomes in patients with HF.