The triglyceride glucose index predicts short-term mortality in non-diabetic patients with acute heart failure.

BACKGROUND: The triglyceride glucose index (TyG) has previously been considered a reliable indicator of insulin resistance (IR) and an independent prognostic predictor in heart failure (HF). OBJECTIVES: To clarify the association between the TyG and short-term death in non-diabetic patients admitted for acute heart failure (AHF). MATERIAL AND METHODS: We examined 886 out of 1620 consecutive AHF patients who were admitted to Shunde Hospital, Southern Medical University, Foshan, China, from June 1, 2014, to June 1, 2022. The median of the patientsf TyG values was used to divide them into 2 groups. The following formula was used to calculate the TyG: ln [fasting triglycerides (mg/dL) ~ fasting glucose (mg/dL)/2]. The data on all-cause mortality of AHF patients during their hospital stay were collected. The 30-day Enhanced Feedback for Effective Cardiac Treatment (EFFECT) death risk score was used to assess the risk of death. RESULTS: The TyG level was positively correlated with a poor AHF prognostic marker (N-terminal B-type natriuretic peptide (NT-proBNP)) (D = 0.207, p < 0.001) and negatively correlated with a protective marker (serum albumin) (D = .0.43, p < 0.001). Higher TyG values were associated with an elevated EFFECT score and hospital mortality (p < 0.001). According to multivariate logistic regression analysis, higher TyG levels raised the risk of death in hospital (odds ratio (OR) = 1.73; 95% confidence interval (95% CI): 1.03.3.27; p = 0.031) after adjusting for multiple variables, including age, EFFECT score and NT-proBNP. The TyG had a greater area under the receiver operating characteristic (ROC) curve (AUC: 0.688) for predicting hospital death compared to NT-proBNP (AUC: 0.506). CONCLUSIONS: Our findings show that the TyG is associated with the short-term mortality rate of non-diabetic patients admitted to the hospital for AHF. The TyG testing could be a useful prognostic indicator for these patients.

Knockdown circ_0040414 inhibits inflammation, apoptosis and promotes the proliferation of cardiomyocytes via miR-186-5p/PTEN/AKT axis in chronic heart failure.

Previous studies have shown that circ_0040414 is highly expressed in the blood of patients with heart failure (HF), which suggests that circ_0040414 is associated with heart failure (HF). However, the functional involvement of circ_0040414 in HF and its potential mechanism remains unclear. Consistent with previous studies, our study showed that the expression of circ_0040414 in the peripheral blood of patients with chronic heart failure (CHF) was significantly higher than that of healthy control, which indicated that circ_0040414 could be used as a diagnostic biomarker in patients with CHF. In cardiomyocytes, circ_0040414 increased the level of proapoptotic proteins Bax, cleaved-caspase 3 and reduced the expression of antiapoptotic protein Bcl-2. It also promoted inflammatory factors IL-6, TNF-α, and IL-ß, but inhibited cell proliferation. In terms of mechanism, circ_0040414 upregulated the expression of phosphatase and tensin homolog (PTEN) through sponging miR-186-5p to inhibit AKT signaling activity. Our study uncovered a novel role and the mechanism of circ_0040414 in controlling CHF, enriched the molecular regulatory network in CHF, and may provide a possible strategy for the treatment of CHF.