The no-reflow (NR) phenomenon is a serious complication of primary percutaneous coronary intervention (PCI) in ST-elevation myocardial infarction (STEMI), often reflecting distal embolization and microvascular obstruction, and representing a substrate for periprocedural (type 4a) myocardial infarction. NR has been linked to worse prognosis, including higher short- and long-term mortality. Inflammation is a key contributor to NR development. This study aimed to evaluate the relationship between the derived neutrophil-to-lymphocyte ratio (dNLR) and NR in STEMI patients undergoing PCI, and to assess its predictive value. This retrospective, single-center observational study included consecutive STEMI patients undergoing primary PCI between May 2024 and May 2025. Patients were grouped based on post-procedural TIMI flow grade. Demographic, clinical, and laboratory parameters were compared. Regression and ROC analyses were performed. A total of 208 patients were analyzed, among whom no-reflow occurred in 26.4% (n = 55). The NR group had significantly higher dNLR, C-reactive protein (CRP), glucose, creatinine, and troponin levels, along with lower left ventricular ejection fraction (LVEF). dNLR, diabetes mellitus, CRP and LVEF were independent predictors of NR. dNLR is a simple, cost-effective marker that may help identify patients at high risk of no-reflow in STEMI. Further prospective studies are warranted.

Purpose: This study aimed to investigate the association between the pan-immune-inflammation value (PIV) and dipper/non-dipper status in newly diagnosed hypertensive (HT) patients. Given the role of systemic inflammation in circadian blood pressure (BP) pattern, we hypothesized that elevated PIV levels would be linked to an impaired nocturnal BP decline. Patients and Methods: A total of 725 newly diagnosed hypertensive patients and 343 normotensive controls were prospectively included in the study. The HT patients were further classified as dipper (n=339) or non-dipper (n=386) based on 24-hour ambulatory BP monitoring (ABPM). PIV was calculated as (neutrophil count × platelet count × monocyte count) / lymphocyte count. Multivariate logistic regression analysis was performed to assess the independent association between PIV quartiles and non-dipper status. Receiver operating characteristic (ROC) curve analysis was conducted to determine the predictive value of PIV. Results: PIV was significantly higher in non-dipper hypertensive patients compared with dipper hypertensive patients (p< 0.001). In multivariate regression models adjusted for age, sex, body mass index (BMI), smoking, diabetes mellitus, and echocardiographic parameters, the highest PIV quartile (Q4) was independently associated with non-dipper status (OR: 12.56, 95% CI: 7.31– 21.56, p< 0.001). ROC analysis demonstrated that a PIV cutoff of 326.96 predicted non-dipper status with a sensitivity of 70.5% and specificity of 65.5% (AUC: 0.725, p< 0.001). Conclusion: Elevated PIV levels were significantly associated with non-dipper hypertension, reinforcing the contribution of systemic inflammation to circadian BP dysregulation. These findings suggest that PIV may serve as a potential biomarker for risk stratification and personalized treatment approaches in hypertensive patients.

Background/Objectives: Metabolic dysfunction-associated fatty liver disease (MAFLD) is linked to cardiovascular complications, including atrial fibrillation. P-wave indices (PWIs) reflect atrial conduction heterogeneity but have not been fully evaluated in MAFLD. To compare PWIs in MAFLD patients versus controls, assess their association with fibrosis severity, and evaluate their diagnostic performance for MAFLD and fibrosis. Methods: In this retrospective single-center study, 447 subjects were included (noMAFLD: Fatty Liver Index (FLI) < 30 without metabolic dysfunction, n = 205; MAFLD: FLI ≥ 60+ ≥ 1 metabolic risk factor, n = 242). Among MAFLD subjects, the non-alcoholic fatty liver disease (NAFLD) Fibrosis Score (NFS) stratified lower (NFS ≤ −1.455; n = 170), and there was a higher fibrosis risk (NFS > −1.455; n = 72). Standard 12-lead ECGs were digitized for offline PWI measurement. Statistical analyzes included group comparisons, multivariable logistic regression, and ROC curve analysis. Results: MAFLD patients exhibited a longer PWPT-D2 (63 ± 12 vs. 52 ± 10 ms, p = 0.003), PWPT-V1 (68 ± 14 vs. 60 ± 13 ms, p = 0.005), PWdis (55 ± 13 vs. 46 ± 11 ms, p = 0.010), and PTFV₁ (38 [31–46] vs. 28 [22–34] mm·ms, p = 0.021) compared with controls. Within MAFLD, a higher fibrosis risk was associated with a further PWI prolongation (all p < 0.015). Multivariate analysis identified PWPT-D2 (OR 1.05 per ms; 95% CI 1.02–1.08; p = 0.002) and PWDIS (OR 1.03 per ms; 95% CI 1.00–1.06; p = 0.048) as independent MAFLD predictors. ROC curves showed PWPT-D2 had the highest AUC for MAFLD detection (0.78; 95% CI 0.72–0.84) and fibrosis (0.82; 95% CI 0.76–0.88). Combining PWPT-D2 with BMI and waist circumference improved MAFLD discrimination (AUC 0.89; 95% CI 0.85–0.93; p < 0.001 vs. PWPT-D2 alone). Conclusions: PWPT-D2 and PWdis are significantly prolonged in MAFLD and more so with advanced fibrosis. PWPT-D2 may be a simple, noninvasive ECG marker for MAFLD screening and fibrosis staging, particularly when combined with anthropometric measures.

No-reflow phenomenon (NR) is a serious complication with increased morbidity and mortality in percutaneous coronary interventions in patients with acute ST-segment elevation myocardial infarction (STEMI). Studies on the relationship between the NR and mean platelet volume (MPV) and platelet count (PLT) are controversial. Platelet mass index (PMI) is a novel inflammation and platelet index, calculated as PLT multiplied by MPV. So, it would be prudent to assume that a high PMI is likely to be associated with NR. PMI’s low cost and rapid availability may aid NR risk stratification. Our aim was to assess the relationship between PMI and no-reflow in acute STEMI patients. A total of 212 acute STEMI patients were enrolled in this retrospective study and the patients were stratified into two subgroups as no-reflow group (n = 45) and reflow group (n = 167). Patient data regarding demographics, clinical, angiographic and laboratory parameters were retrieved from the digital hospital archives. No-reflow was defined angiographic thrombolysis in myocardial infarction (TIMI) flow grade ≤ 2. PMI was calculated as platelet count multiplied by mean platelet volume (MPV). Mean age of the no-reflow and reflow groups was 59.3 ∓ 8.6 and 59.1 ∓ 12.6 years, respectively (p > 0.05). PMI was greater in the no-reflow group [2585(2278–3000) vs. 2054(1594–2344), respectively, p < 0.001]. PMI was correlated with WBC count (r = 0.290, p < 0.001), Hemoglobin (r=-0.281, p < 0.001), neutrophil count (p = 0.303, p < 0.001), platelet count (r = 303, p < 0.001), MPV (r = 0.195, p = 0.006), platelet distribution width (p = 0.215, r = 0.002), and PCT (r = 0.970, p < 0.001), and Syntax score-2 (r = 0.162, p = 0.024). In mulvariate logistic regression analysis, PMI [OR: 1.008(1.003–1.012), p = 0.001], age [OR: 1.111 (1.036–1.253), p = 0.007], and WBC count [OR: 0.018(0.001–0.581), p = 0.024] were independently associated with NR. PMI has been a simple and readily available parameter that could be a promising indicator to estimate NR in patients with acute STEMI.

Objective: Myocardial infarction has unfavorable effect on structural and functional properties of the myocardium, referred to as cardiac remodeling. Left ventricular mass, left ventricular mass index, and relative wall thickness are important predictors of cardiac remodeling. In this study, we investigated the effect of candesartan treatment in comparison with zofenopril treatment on echocardiographic indices of cardiac remodeling in post myocardial infarction patients. Material and Methods: In this prospective study, patients who underwent successful percutaneous coronary intervention were randomly assigned to a candesartan or zofenopril treatment. After randomization, echocardiographic indices of cardiac remodeling including left ventricular mass, left ventricular mass index, and relative wall thickness were evaluated before the start of treatment along with 1 -and 6-month follow-ups. Results: According to our study, candesartan group showed significant reduction of estimated left ventricular mass and left ventricular mass index at 6-month follow-up visit compared to baseline values (199.53 +/- 38.51 g vs. 212.69 +/- 40.82 g; 99.05 g/m(2) (90.00-116.5) vs. 106.0 g/m(2) (96.0 similar to 123.00), p<0.05, respectively). This trend was also observed in zofenopril group during the 6-month period (201.22 +/- 40.07 g vs. 207.52 +/- 41.61 g; 101.0 g/ m(2) (92.25-111.75.0) vs. 104.50 g/m(2) (95.0 similar to 116.75), p<0.05, respectively). Although both classes of drugs had favorable effects on post-myocardial infarction cardiac remodeling, the absolute benefit was more prominent in candesartan group as compared to zofenopril group (p<0.05). Conclusion: Our results suggest that candesartan treatment following myocardial infarction may potentially be useful in terms of improving post -myocardial infarction cardiac remodeling.