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: Low‐voltage areas (LVAs) identified by electroanatomical mapping are commonly used to characterize the atrial substrate in persistent atrial fibrillation (PeAF). However, voltage measurements may vary according to rhythm and physiological state, and LVAs should not be considered synonymous with histological scar or fibrosis. Objective: To evaluate rhythm‐ and physiological state‐dependent changes in left atrial LVAs during atrial fibrillation (AF), early sinus rhythm after cardioversion (SR1), and sinus rhythm under isoproterenol infusion (SR2). Methods: This retrospective observational study included 49 patients with persistent AF undergoing first‐time catheter ablation. High‐density left atrial voltage maps were acquired during AF, early sinus rhythm after electrical cardioversion (SR1), and sinus rhythm during isoproterenol infusion (SR2). Bipolar LVAs were defined as voltage amplitudes < 0.3 mV during AF and < 0.5 mV during sinus rhythm. Unipolar LVAs were defined using corresponding rhythm‐specific thresholds of < 0.71 mV during AF and < 0.83 mV during sinus rhythm, whereas dense bipolar LVAs were defined as bipolar voltage amplitudes < 0.2 mV. Global and regional LVA burden was quantified, and complete paired global analyses included 48 patients. Results: Global LVA burden decreased stepwise across mapping conditions. Bipolar LVA ratio decreased from 17.25% (IQR, 11.40–31.76) during AF to 8.70% (IQR, 6.98–16.17) during SR1 and 5.20% (IQR, 2.60–10.93) during SR2 ( p < 0.001). Similar reductions were observed for unipolar and dense bipolar LVA ratios (both p < 0.001). Regional analysis showed significant heterogeneity in bipolar LVA reduction, whereas unipolar and dense bipolar changes were more homogeneous. Larger left atrial volume was associated with less pronounced bipolar and unipolar LVA reduction. AF duration category was not significantly associated with LVA reduction. Conclusion: Voltage‐defined LVAs in PeAF vary substantially according to rhythm and physiological state. These findings suggest that single‐condition voltage mapping may incompletely characterize the atrial substrate and should be interpreted as dynamic electroanatomical changes rather than evidence of fibrosis or scar regression.

Aim . Тo evaluate the impact of intensive statin therapy on subclinical left (LV) and right ventricular (RV) function using advanced speckle-tracking echocardiography (STE) in patients without coronary artery disease receiving statin for primary prevention. Material and methods. This single-center prospective study enrolled patients who were planned to initiate high-intensity statin therapy (atorvastatin 40-80 mg or rosuvastatin 20-40 mg) for primary prevention. A total of 38 patients (mean age 51.5±7.6 years; 36.8% male) with low-density lipoprotein cholesterol (LDL-C) levels ≥160 mg/dl and no history of coronary artery disease, heart failure, or hypertension were included. Conventional echocardiography and two-dimensional STE were performed at baseline (before therapy initiation) and at a 6-month follow-up. LV global longitudinal strain (LV-GLS) and RV global longitudinal strain (RV-GLS) were calculated to detect subtle myocardial changes. Results . After six months of intensive therapy, a significant reduction in LDL-C (200.5±39.8 to 97.5±29.3 mg/dl; p<0.001) and triglycerides (p=0.001) was observed. Despite significant increases in creatine kinase (p=0.014) and liver enzymes (asparagine aminotransferase: p=0.049, alanine aminotransferase: p=0.036) within the normal-to-borderline range, no clinical myopathy occurred. Echocardiographic analysis showed no significant differences in LV-GLS (-19.2±2.3% vs. -19.4±1.7%; p=0.569) or RV-GLS (-19.2±4.2% vs. -19.5±4.4%; p=0.553) between baseline and follow-up. Similarly, diastolic function parameters (e’, E/e’ ratio) and ejection fraction remained stable throughout the study period. Conclusion . Six months of high-dose statin therapy did not significantly alter biventricular strain parameters in patients without preexisting coronary artery disease. These findings suggest that intensive short-term statin use is not associated with adverse effects on myocardial mechanical function. The stability of strain values, despite lipid reduction and mild enzyme elevations, supports the myocardial safety profile of intensive statin therapy in a primary prevention population.