RESUMEN
BACKGROUND: To develop a prediction model for in-hospital mortality of patients with heart failure (HF) and atrial fibrillation (AF). METHODS: This cohort study extracted the data of 10,236 patients with HF and AF upon intensive care unit (ICU) from the Medical Information Mart for Intensive Care (MIMIC). The subjects from MIMIC-IV were divided into the training set to construct the prediction model, and the testing set to verify the performance of the model. The samples from MIMIC-III database and eICU-CRD were included as the internal and external validation set to further validate the predictive value of the model, respectively. Univariate and multivariable Logistic regression analyses were used to explore predictors for in-hospital death in patients with HF and AF. The receiver operator characteristic (ROC), calibration curves and the decision curve analysis (DCA) curves were plotted to evaluate the predictive values of the model. RESULTS: The mean survival time of participants from MIMIC-III was 11.29 ± 10.05 days and the mean survival time of participants from MIMIC-IV was 10.56 ± 9.19 days. Simplified acute physiology score (SAPSII), red blood cell distribution width (RDW), beta-blocker, race, respiratory rate, urine output, coronary artery bypass grafting (CABG), Charlson comorbidity index, renal replacement therapies (RRT), antiarrhythmic, age, and anticoagulation were predictors finally included in the prediction model. The AUC of our prediction model was 0.810 (95%CI: 0.791-0.828) in the training set, 0.757 (95%CI: 0.729-0.786) in the testing set, 0.792 (95%CI: 0.774-0.810) in the internal validation set, and 0.724 (95%CI: 0.687-0.762) in the external validation set. The calibration curves of revealed that the predictive probabilities of our model for the in-hospital death in patients with HF and AF deviated slightly from the ideal model. The DCA curves revealed that the use of our prediction model increased the net benefit than use no model. CONCLUSION: The prediction model had good discriminative ability, and might provide a tool to timely identify patients with HF complicated with AF who were at high risk of in-hospital mortality.
Asunto(s)
Fibrilación Atrial , Insuficiencia Cardíaca , Humanos , Fibrilación Atrial/diagnóstico , Fibrilación Atrial/terapia , Mortalidad Hospitalaria , Estudios de Cohortes , Insuficiencia Cardíaca/diagnóstico , Insuficiencia Cardíaca/terapia , Antiarrítmicos , Unidades de Cuidados IntensivosRESUMEN
BACKGROUND: Hypoxia could induce cardiomyocytes injury and lead to heart disease. Studies have shown that 6-Gingerol has a protective effect on cardiomyocytes injury, but its molecular mechanism is still unclear. METHODS: Cell counting kit 8 (CCK8) and flow cytometry assays were used to measure the viability and apoptosis of cardiomyocytes. Western blot (WB) analysis was performed to assess the levels of proliferation, apoptosis, and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway-related proteins. The reactive oxygen species (ROS) level, superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were detected by their corresponding Assay Kits. Besides, the expression levels of potassium voltage-gated channel subfamily Q member 1 opposite strand 1 (KCNQ1OT1) and microRNA-340-5p (miR-340-5p) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Furthermore, dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to verify the interaction between KCNQ1OT1 and miR-340-5p. RESULTS: Hypoxia could inhibit the viability and enhance the apoptosis and oxidative stress of cardiomyocytes to induce cardiomyocytes injury, while 6-Gingerol could alleviate this effect. Overexpression of KCNQ1OT1 aggravated hypoxia-induced cardiomyocytes injury and reversed the protective effect of 6-Gingerol on cardiomyocytes injury. Besides, miR-340-5p could be sponged by KCNQ1OT1, and its overexpression could invert the promotion effect of KCNQ1OT1 overexpression on hypoxia-induced cardiomyocytes injury. Moreover, miR-340-5p expression was regulated by 6-Gingerol and KCNQ1OT1. In addition, hypoxia inactivated the PI3K/AKT signaling pathway, whereas 6-Gingerol and miR-340-5p could reverse this effect. CONCLUSIONS: 6-Gingerol could hinder the expression of KCNQ1OT1 to protect cardiomyocytes from hypoxia-induced injury through regulation of the miR-340-5p/ PI3K/AKT pathway, providing a new mechanism of 6-Gingerol protecting cardiomyocytes from injury.