Background: The American Heart Association has modified Life's Essential 8 (LE8) as a new algorithm for evaluating cardiovascular health (CVH). However, the relationship between LE8 and cardiovascular disease (CVD) incidence among diabetic patients, and the potential effect of oxidative stress and inflammation within these associations remain to be elucidated.
Methods: Three thousand eight hundred twenty-eight diabetic patients were selected from the National Health and Nutrition Examination Survey (NHANES). The weighted logistic regression was employed to examine the association between LE8 with CVD, and the quantitative relationship was investigated with a restricted cubic spline (RCS). Mediation analyses explored the mediating role of oxidative stress and inflammation in the above relationship.
Results: In the 3828 diabetic patients, a total of 977 people were diagnosed with CVD, and the LE8 was significantly and linearly negatively associated with CVD incidence. After all covariates were adjusted, the medium CVH group had a 25% lower risk of CVD (OR: 0.75, 95% CI: 0.58, 0.95) than the low CVH group, and the high CVH group had a 66% lower risk (OR: 0.34, 95% CI: 0.12, 0.94). Furthermore, oxidative stress and inflammation explained 11.57% and 10.89% of the connection, respectively (P<0.05).
Conclusion: Elevated LE8 is negatively associated with adverse cardiovascular events in diabetes mellitus and the association appeared to be partially mediated through oxidative stress and inflammation pathways. Those results indicate the necessity of maintaining at least moderate cardiovascular health and the LE8 help make lifestyle self-management more targeted for diabetes patients.
Background: MicroRNAs (miRs) regulate gene expression post-transcriptionally and are transported by high-density lipoproteins (HDL). Hypercholesterolemic HDL particles are enriched with miR-126-3p/5p, which can be delivered to endothelial cells, leading to the downregulation of hypoxia-inducible-factor-1α (HIF-1α), a key transcription factor involved in metabolic responses to hypoxia and cell survival during myocardial ischemia/reperfusion (I/R).
Objective: To investigate the effects of miR-126 mimic and inhibitor transfection on the HIF-1α/apoptosis axis in cardiac cell constituents under experimental I/R.
Methods: Firstly, specific durations of I/R were established for cardiac cells (cardiomyocytes, fibroblasts, endothelial cells, and macrophages) based on their susceptibility to metabolic changes and cell death. Then, we assessed the impact of transfecting these cells with mimic-miR-126-5p and anti-miR-126-5p to the selected timings of I/R on the HIF-1α/apoptosis axis.
Results: Endothelial cells were resistant to I/R and fibroblasts were sensitive to ischemia whereas cardiomyocytes displayed high metabolic flexibility. Endogenous miR-126 expression was exclusively found in endothelial cells. Transfection with anti-miR-126 increased HIF-1α transcription in endothelial cells and cardiomyocytes, while reducing HIF-1α levels in fibroblasts, resulted in decreased transcript levels of apoptotic markers. HIF-1α transcript levels remained unchanged in macrophages and transfection with mimic-miR-126 exerted no changes in the HIF-1α/apoptosis axis in all tested cells.
Conclusions: miR-126 differentially regulates HIF-1α/apoptosis expression in cardiac cells exposed to experimental I/R and may serve as a potential therapeutic target for enhancing myocardial resilience in the setting of myocardial infarction.
Objective: The neutrophil percentage-to-albumin ratio (NPAR) is a readily available biomarker with prognostic significance across various disease conditions. However, its role in predicting mortality among community patients with chest pain remains underexplored. This study examined NPAR's association with long-term mortality in adults with chest pain using NHANES 2001-2018 data.
Methods: We analyzed data from 6846 community-dwelling adults reporting chest pain. Cox proportional hazards regression models, restricted cubic spline (RCS) analysis, and Kaplan-Meier survival curves were employed to evaluate the relationship between NPAR and the risk of all-cause and cardiovascular mortality. Models were adjusted for demographic, clinical, and laboratory covariates.
Results: Participants were categorized into tertiles based on NPAR values: T1 (<13.0), T2 (13.0-15.0), and T3 (>15.0). Multivariable analysis revealed that the T3 cohort demonstrated significantly increased risks of all-cause mortality (HR 1.56, 95% CI 1.32-1.84, P<0.001) and cardiovascular mortality (HR 1.86, 95% CI 1.37-2.51, P<0.001) relative to T1. RCS analysis identified a J-shaped relationship between NPAR and mortality risk, with a significant inflection point at NPAR >13.5 (P for non-linearity <0.001). Incremental analysis showed that each unit increase in NPAR was associated with an 11% higher risk of all-cause mortality (HR 1.11, 95% CI 1.07-1.14, P<0.001) and a 14% increased risk of cardiovascular mortality (HR 1.14, 95% CI 1.08-1.20, P<0.001).
Conclusions: Elevated NPAR levels are independently associated with increased long-term mortality in adults with chest pain. These findings position NPAR as a promising prognostic biomarker in this patient population.
Aims: SCORE2 and SCORE2-OP cardiovascular risk tables were published in 2021 and incorporated into European cardiovascular prevention guidelines, replacing the previous SCORE tables. Since the 2012 version of these guidelines, the concept of vascular age has been included. Although there are vascular age tables derived from SCORE, there are no vascular age tables derived from SCORE2 and SCORE2-OP. The aim of this study is to construct new vascular age tables derived from SCORE2 and SCORE2-OP.
Methods: Based on the data from the SCORE2 and SCORE2-OP risk tables, 8 regressions between age and risk are calculated in baseline conditions for the 8 combinations of sex and cardiovascular risk zones. Another 248 regressions corresponding to the different non-baseline situations are calculated. By equating the risk in each box of the risk tables with the same risk in baseline conditions, the vascular age in each box of the risk tables can be obtained. Regression, determination and intraclass correlation coefficients are calculated to asses adjustment and agreement.
Results: Four vascular age tables have been obtained corresponding to countries with low, moderate, high and very high cardiovascular risk. The concordance in vascular age between the 4 tables is greater than 0.99, thus a universal vascular age table has been constructed. Vascular age does not need calibration unlike absolute risk.
Conclusions: Vascular age tables have been created from the SCORE2 and SCORE2-OP tables. A single vascular age table may be used for all European Countries.
Objective: To analyze lipid profiles and sociodemographic factors associated with atherogenic risk in obese workers classified as metabolically healthy (MHO) or unhealthy (MNHO).
Methods: Cross-sectional study of 68,884 obese workers. Atherogenic lipid indices (total cholesterol/HDL-c, LDL-c/HDL-c, triglycerides/HDL-c) and prevalence of atherogenic dyslipidemia were assessed. Multinomial logistic regression identified factors linked to lipid risk.
Results: MNHO individuals exhibited significantly higher atherogenic indices across sexes and diagnostic criteria. Atherogenic dyslipidemia and lipid triad were more prevalent in MNHO. Male sex, older age, lower educational level, lower social class, physical inactivity, low adherence to the Mediterranean diet, and smoking were associated with higher lipid risk.
Conclusion: Although MHO individuals show a more favorable lipid profile than MNHO, this advantage weakens with less stringent definitions. Sociodemographic and lifestyle factors strongly modulate atherogenic risk.

