Heart failure (HF) remains a significant health problem despite advances in diagnosis and treatment options. Malnutrition and increased inflammation predict poor disease prognosis. The parameters of the Naples prognostic score (NPS) include albumin, total cholesterol, neutrophil-lymphocyte ratio (NLR), and lymphocyte-monocyte ratio (LMR). We aimed to assess the potential of NPS as a predictor of long-term mortality in patients with HF. A total of 1728 patients with HF who applied to our center between 2018 and 2022 were included in this study. The NPS was computed and the patients were divided into three groups according to their NPS values as follows: NPS = 0 (Group 1), NPS = 1-2 (Group 2), and NPS = 3-4 (Group 3). We also evaluated the association between NPS value and HF mortality. The patients were followed for a mean follow-up duration of 30 months. The mortality rate was 8.3% (145 patients). We carried out Model-1 and -2 Cox regression analyses to identify long-term mortality determinants. Model-2 was constructed by adding NPS to Model-1. NPS was significantly associated with HF mortality (Hazard Ratio: 2.194, 95% Confidence Interval: 1.176-4.091, p = 0.014). According to the Kaplan-Meier plot and log-rank analyses, there was a statistically significant difference in the long-term mortality of patients with HF and their NPS values for the entire cohort. Based on our findings, NPS showed promise as an independent predictor of long-term mortality in individuals with HF.

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.

The systemic immune-inflammation index (SII), a novel marker derived from the combination of platelet, neutrophil, and lymphocyte counts, has been linked to unfavorable clinical outcomes in various malignancies and inflammatory conditions. This study aims to assess the association between SII and disease prognosis in patients with heart failure with reduced ejection fraction (HFrEF). A total of 521 patients (72% male; mean age: 67 ± 13 years) diagnosed with HFrEF were retrospectively analyzed. Clinical, demographic, laboratory, and echocardiographic data were collected. SII scores were calculated for all patients, and their prognostic significance and clinical outcomes were evaluated. 521 patients were analyzed. According to current findings, all-cause mortality occurred in 87 patient during the follow-up period. The mean SII in the mortality group was higher than in the survivors and was found to be statistically significant. (878.57 vs. 643.65; p = 0.003, respectively) In the multivariable regression model SII was found to be an independent risk factor for mortality. (p = 0.031) The AUC of SII for mortality prediction was 0.602 (95% CI = 0.531–0.673), the cut-off value was 729, and the sensitivity and specificity were 59.3% and 59.6% (p = 0.003). This study demonstrates a significant association between SII and both survival and prognosis in patients with HFrEF. Notably, the SII index was found to be an independent predictor of mortality in this patient population.

Background Dual antiplatelet therapy (DAPT) is the treatment of choice for patients with acute and chronic coronary syndromes as it reduces mortality and prevents recurrent thrombotic complications. The assessment of both ischaemic burden and bleeding risk is crucial in deciding which DAPT to choose and how long it should be continued. Objectives The aim of our study was to perform prospective clinical follow-up of patients receiving fixed-dose combination therapy (ASA 75 mg + clopidogrel 75 mg). Our study is a multicentric, cross-sectional, observational, cohort study. Methods A total of 1500 patients who were started on fixed-dose combination DAPT for acute or chronic coronary syndrome were included in the study. Primary endpoints were hospitalization for any reason, hospitalization for cardiovascular cause, acute myocardial infarction, stent thrombosis, target vessel revascularization and bleeding; the secondary endpoints were death for any reason or cardiovascular cause and stroke. The significance level adopted in the statistical analysis was 5%. Results Median age was 63 years; 78.5% of the patients were receiving DAPT treatment for acute coronary syndrome. The rates of hospitalization for cardiovascular reasons, acute myocardial infartion, stent thrombosis and target-vessel revascularization were 7.9%, 2.3%, 1.3% and 4.2%, respectively. While the rate of BARC type 1 bleeding was 3.3%, the rate of BARC type 5, 3, or 2 bleeding was 0.6%. The secondary endpoints which were death from any cause, cardiovascular death and stroke were 0.5%, 0.3% and 0.3%, respectively. Conclusion: Our study shows that fixed-dose combination therapy is effective and safe in appropriately selected patients with acute or chronic coronary syndromes.

Background: There is limited data in the literature about the clinical importance and prognosis of pericardial effusion (PE) in patients discharged after recovering from COVID-19, but large-scale studies have yet to be available. This study investigated the prevalence, risk factors, prognosis, late clinical outcomes, and management of PE in COVID-19. Materials and Methods: Between August 2020 and March 2021, 15,689 patients were followed up in our pandemic hospital due to COVID-19. Patients with positive polymerase chain reaction (PCR) test results and PE associated with COVID-19 in computed tomography (CT) were included in the study. The patients were divided into three groups according to PE size (mild, moderate, and large). Transthoracic echocardiography (TTE) records, laboratory data, clinical outcomes, and medical treatments of patients discharged from the hospital were retrospectively reviewed. Results: According to the PE size (mild, moderate, large) of 256 patients with PE at admission or discharge, the mean age was 62.17 ± 16.34, 69.12 ± 12.52, and 72.44 ± 15.26, respectively. The mean follow-up period of the patients was 25.2 ± 5.12 months. Of the patients in the study population, 53.5% were in the mild group, 30.4% in the moderate group, and 16.1% in the large group. PE became chronic in a total of 178 (69.6%) patients at the end of the mean three months, and chronicity increased as PE size increased. Despite the different anti-inflammatory treatments for PE in the acute phase, similar chronicity was observed. In addition, as the PE size increased, the patients’ frequency of hospitalization, complications, and mortality rates showed statistical significance between the groups. Conclusions: The clinical prognosis of patients presenting with PE was quite poor; as PE in size increased, cardiac and noncardiac events and mortality rates were significantly higher. Patients with large PE associated with COVID-19 at discharge should be monitored at close intervals due to the chronicity of PE and the increased risk of tamponade.

Aortic aneurysm is a vascular disease with a complex pathogenesis which is usually asymptomatic but can lead to high mortality with sudden rupture. This review comprehensively examines the molecular mechanisms of aortic aneurysms in the context of extracellular matrix destruction, smooth muscle cell apoptosis, chronic inflammation, oxidative stress, genetic mutations, and epigenetic regulations. In addition, the potential of molecular biomarkers in diagnosis and prognosis and targeted treatment strategies are evaluated. Animal models and translational findings form the basis for establishing a bridge between preclinical and clinical applications. This study aims to provide insight into the integration of molecular findings into clinical practice in light of the current literature and to guide future research.