Association between the triglyceride glucose (TyG) index and the risk of acute kidney injury in critically ill patients with heart failure: analysis of the MIMIC-IV database.

BACKGROUND: Insulin resistance (IR) can be effectively assessed using the dependable surrogate biomarker triglyceride-glucose (TyG) index. In various critical care contexts, like contrast-induced acute kidney injury (AKI), an elevated TyG index has demonstrated a robust correlation with the incidence of AKI. Nonetheless, the potential of the TyG index to predict AKI in critically ill patients with heart failure (HF) remains uncertain. METHODS: A cohort of participants was non-consecutively selected from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database and divided into quartiles based on their TyG index values. The incidence of AKI was the primary outcome. The secondary endpoint was in-hospital mortality within both the whole study population and the subset of AKI patients. The use of the renal replacement therapy (RRT) which represented the progression of AKI severity was also included as a secondary endpoint representing renal outcome. A restricted cubic splines model and Cox proportional hazards models were utilized to evaluate the association of TyG index with the risk of AKI in patients with HF in a critical condition. Kaplan-Meier survival analysis was employed to estimate primary and secondary endpoint disparities across groups differentiated by their TyG index. RESULTS: This study included a total of 1,393 patients, with 59% being male. The incidence of AKI was 82.8%. Cox proportional hazards analyses revealed a significant association between TyG index and the incidence of AKI in critically ill patients with HF. The restricted cubic splines model illustrated the linear relationship between higher TyG index and increased risk of AKI in this specific patient population. Furthermore, the Kaplan-Meier survival analyses unveiled statistically significant differences in the use of RRT across the subset of AKI patients based on the quartiles of the TyG index. CONCLUSIONS: The results highlight the TyG index as a robust and independent predictor of the incidence of AKI and poor renal outcome in patients with HF in a critical condition. However, further confirmation of causality necessitates larger prospective studies.

Prognostic value of red cell distribution width in patients undergoing percutaneous coronary intervention: a meta-analysis.

OBJECTIVE: To evaluate the prognostic value of baseline red cell distribution width (RDW) in patients with coronary artery diseases (CADs) undergoing percutaneous coronary intervention (PCI) by conducting a meta-analysis. DESIGN: Systematic review and meta-analysis. DATA SOURCE: PubMed, Embase, Wanfang, CNKI and VIP databases were searched from their inceptions to 19 June 2019. ELIGIBLE CRITERIA: Studies investigating the value of baseline RDW for predicting all-cause mortality, cardiovascular mortality and major adverse cardiac events (MACEs) in patients with CAD undergoing PCI were included. DATA EXTRACTION AND SYNTHESIS: Two authors independently extracted the data and evaluated the methodological quality using the Newcastle-Ottawa Scale. STATA V.12.0 software was applied to produce the forest plots using a random-effect model. RESULTS: Twelve studies (13 articles) involving 17 113 patients were included and analysed. Comparison between the highest and lowest RDW category indicated that the pooled risk ratio (RR) was 1.77 (95% CI 1.32 to 2.37) for all-cause mortality, 1.70 (95% CI 1.25 to 2.32) for cardiovascular mortality and 1.62 (95% CI 1.21 to 2.18) for MACEs. The predictive effect of elevated RDW for all-cause mortality was stronger in the subgroup of patients without anaemia (RR 4.59; 95% CI 3.07 to 6.86) than with anaemia. CONCLUSIONS: This meta-analysis indicated that elevated RDW was associated with higher risk of mortality and adverse cardiac events in patients with CAD undergoing PCI. The value of elevated RDW for predicting all-cause mortality appears to be stronger in patients without anaemia. RDW may be served as a promising prognostic biomarker in patients undergoing PCI.

Adeno-associated Virus 9-mediated Small RNA Interference of TLR4 Alleviates Myocardial Ischemia and Reperfusion Injury by Inhibition of the NF-κB and MAPK Signaling Pathways in Rats.

BACKGROUND: Despite intensive investigation, effective therapeutic procedures for myocardial I/R injury are still in demand. OBJECTIVE: To explore the effect of adeno-associated virus 9 (AAV9)-mediated small interfering RNA targeting TLR4 in the treatment of myocardial ischemia and reperfusion (I/R) injury and its influence on the NF-κB and MAPK signaling pathways. METHODS: Rats were divided into 3 groups, namely, the sham, AAV9-siRNA control, and AAV9-TLR4 siRNA groups. siRNA solution or normal saline was injected through the tail vain. The rat myocardial I/R injury model was then established. HE staining and TUNEL staining were applied to compare the pathological changes in cardiomyocytes in the three groups. Immunohistochemical staining and western blotting were utilized to detect TLR4 expression under siRNA interference. Serum inflammatory factor (IL-1ß, TNF-α) expression was determined by an ELISA commercial kit. Key proteins in the MAPK (p38, JNK 1/2) and NF-κB (p65) signaling pathways were determined to identify the TLR4 siRNA functional mechanism. RESULTS: Fluorescence microscopic images of the myocardium indicated that AAV9- mediated siRNA was efficiently transfected into the myocardium, and the infarcted size after I/R injury was decreased by AAV9-TLR4 siRNA when compared with negative control rats (P<0.05). TLR4 protein expression was significantly decreased by siRNA interference (P<0.001). Apoptosis-related factor BCL-2 expression was increased in the TLR4 gene silencing group, whereas Bax expression was decreased. The Bax/BCL-2 ratio was also decreased, demonstrating a protective effect for cardiomyocytes. Inflammatory factors were lower in the TLR4 gene silencing group than in the siRNA control group (P<0.001). The MAPK and NF-κB signaling pathways were activated in myocardial I/R injury; however, the primary proteins in these two signaling pathways were downregulated upon interference of TLR4 siRNA, with significant differences (P<0.05). CONCLUSION: AAV9-TLR4 siRNA has a positive effect on myocardial I/R injury by inhibiting the MAPK and NF-κB signaling pathways and can be used as a potential therapeutic method for myocardial I/R injury.