Background: Early risk stratification in acute decompensated heart failure with reduced ejection fraction (ADHF-rEF) remains challenging. The Endothelial Activation and Stress Index (EASIX)—a composite of lactate dehydrogenase, creatinine, and platelet count—reflects endothelial dysfunction, a pathophysiological contributor to early deterioration in ADHF-rEF. This study evaluated the prognostic utility of admission-based EASIX for in-hospital mortality. Methods: In this retrospective single-center cohort, 850 consecutive patients hospitalized with ADHF-rEF between January 2022 and June 2025 were analyzed. EASIX was calculated from first-day laboratory values. Logistic regression, ROC analysis, restricted cubic splines, and Kaplan–Meier survival methods were used to assess the association between EASIX and in-hospital mortality, and to evaluate its incremental value beyond established clinical and laboratory predictors. Results: In-hospital mortality was 12.4%. Higher EASIX values were significantly associated with mortality in both univariable and multivariable models (adjusted OR 1.273; p < 0.001). EASIX demonstrated moderate discriminative performance among evaluated biomarkers (AUC 0.751) and showed a clear dose–response risk gradient, with mortality rising from 1.4% in the lowest tertile to 26.2% in the highest. Incorporating EASIX into clinical and laboratory prediction models yielded substantial continuous net reclassification improvement (0.59 and 0.38, respectively). Survival curves diverged early and remained distinctly separated across EASIX strata. Conclusions: Admission EASIX is an independent predictor of in-hospital mortality in ADHF-rEF and provides complementary prognostic information beyond conventional models. This is the first study to demonstrate the prognostic value of EASIX in the ADHF-rEF setting, supporting its potential utility as an accessible endothelial stress biomarker for early risk stratification.

Cardiovascular diseases (CVDs) are the leading cause of global morbidity and mortality, with oxidative stress and redox imbalance playing pivotal roles in their initiation and progression. In this comprehensive review, we explore the molecular mechanisms by which reactive oxygen and nitrogen species disrupt vascular homeostasis, promote endothelial dysfunction, and drive adverse cardiac remodeling. We highlight key redox-sensitive pathways, including NADPH oxidase activation, mitochondrial dysfunction, endothelial nitric oxide synthase uncoupling, and endoplasmic reticulum stress. Emerging oxidative stress biomarkers, such as 8-iso-prostaglandin F2α, oxidized low-density lipoprotein, and myeloperoxidase, are critically examined for their diagnostic and prognostic relevance. Additionally, we discuss therapeutic strategies targeting oxidative stress, ranging from conventional antioxidants to novel mitochondrial-directed and enzyme-specific interventions. Despite advances in understanding the redox landscape of CVDs, challenges remain in translating these insights into effective clinical therapies. Future research integrating omics technologies, precision medicine, and combined lifestyle-pharmacological approaches may offer new opportunities for redox-based cardiovascular interventions.

Background: Early risk stratification in ST-elevation myocardial infarction (STEMI) remains critical, particularly for anticipating adverse outcomes such as the coronary no-reflow phenomenon (NRP) and early mortality. The Endothelial Activation and Stress Index (EASIX), calculated from routine laboratory parameters, has emerged as a potential biomarker reflecting systemic endothelial dysfunction. This study evaluated the prognostic value of admission EASIX for the NRP and in-hospital mortality in STEMI patients undergoing primary percutaneous coronary intervention (pPCI). Methods: In this retrospective single-center cohort, 1931 STEMI patients treated with pPCI between January 2023 and January 2025 were included. EASIX was calculated at admission. NRP was defined as post-PCI TIMI flow ≤ 2 or TIMI 3 flow with impaired myocardial blush (TMPG ≤ 1). Multivariable logistic regression, reclassification analyses (NRI/IDI), ROC analysis, and calibration methods were used to assess predictive performance. Sensitivity and interaction analyses were conducted. Results: NRP occurred in 14.1%, and in-hospital mortality was 2.5%. EASIX was independently associated with both outcomes (NRP: adjusted OR 1.485, 95% CI 1.286–1.715; mortality: adjusted OR range 1.371–2.096 across models; all p < 0.001). EASIX significantly improved risk reclassification for both NRP and in-hospital mortality (NRI > 0.20). ROC-AUCs were 0.706 for NRP and 0.810 for mortality. Restricted cubic spline and LOWESS analyses revealed nonlinear risk escalation. Calibration plots and Brier scores confirmed model reliability. Associations persisted across ischemic time and renal function strata. Conclusions: Admission EASIX is independently associated with NRP and in-hospital mortality in STEMI. Easily accessible and integrative, EASIX may enhance early risk stratification. External validation is warranted before clinical implementation.

Background and Objectives: Conventional risk models may not adequately capture key biological determinants of mortality following transcatheter aortic valve implantation (TAVI), such as inflammation, malnutrition, and immune dysfunction. The Osaka Prognostic Score (OPS), incorporating CRP, albumin, and lymphocyte count, may address this gap. We aimed to evaluate the prognostic value of OPS for predicting in-hospital and one-year all-cause mortality after TAVI. Materials and Methods: In this retrospective single-center cohort study, 244 patients who underwent transfemoral TAVI between December 2022 and January 2024 were analyzed. OPS was calculated at baseline (range: 0–3), and its prognostic value for in-hospital and one-year all-cause mortality was evaluated using multivariable Cox regression, ROC analysis, and restricted cubic spline (RCS) modeling. Results: In-hospital and one-year mortality rates were 11.5% and 21.7%, respectively. Higher OPS scores were significantly associated with mortality in both periods. OPS independently predicted in-hospital mortality (HR: 2.018; 95% CI: 1.632–2.521; p = 0.017) and one-year mortality (HR: 2.125; 95% CI: 1.300–3.473; p = 0.003). ROC analysis yielded AUC values of 0.776 and 0.859 for in-hospital and one-year mortality, respectively. Kaplan–Meier curves revealed significantly reduced survival in patients with higher OPS (log-rank p < 0.001), and RCS analysis demonstrated a significant nonlinear association between increasing OPS values and mortality risk (p < 0.001). Conclusions: OPS is a simple, cost-effective, and biologically relevant prognostic index that independently predicts both in-hospital and one-year mortality following TAVI. By integrating markers of inflammation, nutrition, and immune competence, OPS may offer additional value in risk stratification and support clinical decision-making in this high-risk population.