Background and Objectives: Heart failure is a chronic disease with a high risk of mortality and morbidity. In these patients, inflammatory markers have been shown to be associated with cardiovascular adverse outcomes and disease progression. To investigate the relationships between eosinophil indices and major cardiovascular events (MACE) in patients with acute decompensated heart failure (ADHF) with reduced ejection fraction. Materials and Methods: A total of 395 consecutive patients admitted to the intensive care unit (ICU) with ADHF and reduced ejection fraction between January 2017 and December 2021 were enrolled in this retrospective study. MACE was defined as the composite of death and re-hospitalization for ADHF within 6 months of index hospitalization. All-cause mortality and MACE were assessed with respect to relationships with eosinophil indices, including neutrophil-to-eosinophil ratio (NER), leukocyte-to-eosinophil ratio (LER), eosinophil-to-lymphocyte ratio (ELR), and eosinophil-to-monocyte ratio (EMR). Results: NER and LER were significantly higher in subjects with MACE. Absolute eosinophil, lymphocyte and basophil count, hemoglobin, serum Na⁺, albumin, and CRP, and EMR and ELR were significantly lower in subjects with MACE compared to those without. NT-proBNP (OR: 1.682, 95% CI: 1.106–2.312, p = 0.001), Na⁺ (OR: 0.932, 95% CI: 0.897–0.969, p < 0.001), NER (OR: 2.740, 95 % CI: 1.797–4.177, p < 0.001), LER (OR: 2.705, 95% CI: 1.752–4.176, p < 0.001), EMR (OR:1.654, 95% CI 1.123–2.436, p = 0.011), ELR (OR: 2.112, 95% CI 1.424–3.134, p < 0.001), and eosinophil count (OR: 1.833, 95% CI 1.276–2.635) were independent predictors for development of MACE. Conclusions: Patients with ADHF and reduced ejection fraction who developed MACE within the first six months of index hospitalization had lower levels of absolute eosinophil and lymphocyte counts, and EMR and ELR values, whereas NER and LER were higher compared to those without MACE. The eosinophil indices were independently associated with mortality and MACE development. The eosinophil indices may be used to estimate MACE likelihood with acceptable sensitivity and specificity.

Objective Coronary collateral circulation (CCC) are vascular structures that limit the infarct area, protect left ventricular function, and reduce the frequency of arrhythmia and mortality during myocardial ischemia and infarction. In this study, we examined the relationship between the development of CCC and serum adropin levels, which has been shown in previous studies to regulate endothelial functions and increase endothelial nitric oxide synthesis, in patients with acute myocardial infarction. Methods This study included 41 patients with insufficient CCC and 43 patients with well-developed CCC who were hospitalized for acute myocardial infarction and underwent coronary angiography. The Cohen-Rentrop classification was used to grade the CCC. The patients were divided into two groups according to Rentrop grades: those with a 0-1 stage were considered as insufficient and those with grades of 2-3 were considered as well-developed CCC. We took blood samples to measure the adropin levels within the first 24 hours of hospitalization. Results The mean age was 59.1±11.9 years and 62 (73.8%) were male. The right coronary artery was the most frequently target vessel (n: 51, 60.7%), and the majority of the patients presented with ST-segment elevation myocardial infarction (STEMI) (n:58, 69%). The median interval between the severe chest pain and the intervention was significantly higher in patients with well-developed CCC (p=0.042). The serum adropin levels in patients with insufficient CCC were significantly lower than in those with well-developed CCC (196.3 [131.5 - 837.0] pg/mL vs. 235.5 [171.9 - 1124.2] pg/mL, p<0.001). Logistic regression analysis revealed that the circumflex artery as the target vessel, NSTEMI (non-STEMI) as the type of myocardial infarction, and serum adropin level were the independent risk factors for the prediction of poor coronary collateral vessel formation (p<0.05). Conclusions In this study, we found that in patients with acute myocardial infarction, those with well-developed CCC had higher adropin levels.

Prevention of atherosclerotic cardiovascular diseases (ASCVD) is possible with early recognition of individuals at risk. Salusin alpha is an endogenous bioactive peptide with anti-atherogenic properties. We aimed to reveal the relationship between salusin alpha levels and cardiovascular (CV) risk using the Systematic COronary Risk Estimation 2 (SCORE2) and Pooled Cohort Equation (PCE) algorithms. A total of 137 asymptomatic outpatients were included in the study. The participants were divided into four quartile groups according to the distribution of salusin alpha levels: Q1 (n = 34), Q2 (n = 35), Q3 (n = 34), and Q4 (n = 34). The relationships of salusin alpha with cardiovascular risk scores and groups were investigated. The means of SCORE2 and PCE risk scores (11.24 ± 1.24 and 13.30 ± 1.71, respectively; p < 0.001 for both), baseline scores in the presence of SCORE2 and PCE optimal risk factors (4.82 ± 0.71 (p = 0.034); 4.20 ± 0.77 (p = 0.010)), and means of Δ SCORE2 and Δ PCE risk score (6.41 ± 0.67 and 9.10 ± 1.10, respectively; p < 0.001 for both) were significantly higher in the Q1 group. The SCORE2 “very high” cardiovascular (CV) risk group was significantly represented in the Q1 group (n = 17 (50%)), while the “low-moderate” risk group was more heavily represented in the Q4 group (n = 15 (44.1%)) (p < 0.001). The PCE “high” CV risk group was significantly represented in the Q1 group (n = 9 (26.5%)), while the “low” risk group was more intensely represented in the Q4 group (n = 20 (58.8%)) (p < 0.001). Salusin alpha had a significantly negative moderate correlation with SCORE2 and PCE risk scores. As a result of receiver operating characteristic (ROC) analysis, it was found that salusin alpha had significant diagnostic power in the prediction of CV risk groups determined by SCORE2 and PCE risk scores. Salusin alpha was observed to be a risk-reducing factor in SCORE2 and PCE CV risk groups (odds ratio (OR) (95% confidence interval (CI)): 0.989 (0.982-0.997) (p = 0.002) and OR (95% CI): 0.988 (0.978-0.998) (p = 0.009) respectively). Salusin alpha has a negative correlation with SCORE2 and PCE risk scores. It has significant diagnostic power in the prediction of CV risk groups and is an independent variable that has a risk-reducing effect in the distribution of risk groups.

Background: This study investigated the relationship between coronary collateral circulation (CCC) and intracoronary thrombus burden in patients undergoing primary percutaneous coronary intervention for ST-segment elevation myocardial infarction (STEMI). CCC and thrombus burden are predictive of clinical outcomes in patients with STEMI. Methods: Patients with STEMI undergoing primary percutaneous coronary intervention were enrolled (n = 172). CCC was graded according to the Cohen–Rentrop classification. Patients were classified as insufficient (grade 0 or 1, n = 134) or well-developed (grade 2 or 3; n = 38) CCC. The Thrombolysis in Myocardial Infarction scale was used to evaluate intra-coronary thrombus burden. The low-thrombus-burden group comprised those with grades 0 to 2, and the high-thrombus-burden group comprised those with grades 3 or 4. Results: Right coronary artery infarcts had a 13.830-fold higher chance of having well-developed CCC than did left anterior descending artery infarcts (P < .001). Circumflex artery infarcts had a 7.904-fold higher chance of well-developed CCC than did left anterior descending artery infarcts (P = .016). High thrombus burden was associated with a 4.393-fold higher chance for well-developed CCC than was low thrombus burden (P = .030). Low albumin levels were related to a greater chance of having well-developed CCC (P = .046). Conclusion: Patients with well-developed CCC have higher thrombus burden than do those with insufficient CCC. Because well-developed CCC is an indicator of more severe underlying lesions, we speculate that patients with severe lesions are more prone to experience more complicated STEMI with high thrombus burden.

Aims: Resistant hypertension (RHT) accounts for 10-15% of hypertensive patients, and diagnosis and treatment are more complex in these cases, which means a higher risk of cardiovascular complications. Although the effect of chronic systemic inflammation on the pathophysiology of RHT is known, the effective use of biomarkers is limited. This study investigated the relationship between the Systemic Immune-Inflammation Index (SII) and the Systemic Inflammatory Response Index (SIRI), which are composite inflammatory indices that can be used as markers of chronic inflammation, and RHT, testing their clinical utility and predictive value. Methods: Between April 2022 and January 2025, 256 hypertensive patients followed up at our clinic were defined as having controlled hypertension (CHT) and 244 as having RHT, for a total of 500 patients included in this cross-sectional study. SII and SIRI values were calculated from routine blood count results. Data were analyzed and compared using multivariate logistic regression, quartile analysis, limited cubic spline modeling, and receiver operating characteristic (ROC) curve analysis. Results: Significantly higher SII (480.2 vs. 361.7, p

Background: Heart failure with preserved ejection fraction (HFpEF) is increasingly recognized as a systemic multiorgan syndrome driven by low-grade inflammation. While epicardial adipose tissue (EAT) and skeletal muscle dysfunction are known contributors to exercise intolerance, their synergistic association remains undefined. Aims: We aimed to investigate the “Adipo-Muscular” association—the synergistic interplay between local cardiac inflammatory potential and peripheral muscle fatigability—as a predictor of functional capacity in HFpEF. Methods: This cross-sectional study enrolled 192 stable HFpEF patients and 200 age- and sex-matched healthy controls. EAT thickness was quantified via echocardiography. Peripheral muscle function was assessed through maximal isometric strength and handgrip endurance (maintenance time at 50% maximal voluntary contraction), the latter serving as a surrogate for Type I fiber oxidative capacity. Functional capacity was validated using the 6-Minute Pegboard Ring Test (6PBRT), specifically chosen for its sensitivity to upper extremity “myopenia” (qualitative bioenergetic failure). A novel EAT-Endurance Index was calculated as: Index = ({EAT thickness [mm]} / {Handgrip endurance [sec]}) ×100. Results: Despite comparable BMI between groups, HFpEF patients displayed significantly greater EAT thickness (5.46 ± 1.65 vs. 3.20 ± 1.03 mm, p < 0.001). While maximal strength showed a moderate decline, handgrip endurance was profoundly compromised in HFpEF (48.48 ± 14.4 vs. 72.24 ± 12.1 s, p < 0.001), representing a massive effect size (Cohen’s d = -1.791). In multivariate analysis adjusting for age, sex, BMI, and major comorbidities (Hypertension, Diabetes, and Coronary Artery Disease), the EAT-Endurance Index emerged as the strongest independent predictor of impaired functional capacity (β = 0.385, p < 0.001). Sensitivity analysis confirmed this association was independent of glycemic status. Conclusions: We identified a distinct “Adipo-Muscular” phenotype in HFpEF, characterized by expanded epicardial fat and profound skeletal muscle fatigability. This association predicts functional decline independently of systemic obesity, maximal strength, and classic comorbidities. Targeting the interface between central adiposity and skeletal muscle mitochondrial function may offer novel therapeutic avenues for this challenging population.