Interleukin-4 (IL-4) and Interleukin-13 (IL-13) are central regulators of the Th2 immune response and play pivotal roles in vascular inflammation, endothelial dysfunction, and cardiovascular remodeling. While their contributions to immune modulation are well known, their precise effects on the cardiovascular system remain an evolving field of study. This review aims to explore the mechanistic roles of IL-4 and IL-13 in endothelial dysfunction and the development of cardiovascular diseases, and to evaluate the therapeutic potential and risks associated with IL-4/IL-13 inhibitors. A narrative review approach was used. Articles published between 2015 and 2025 were identified through PubMed, Scopus, and Google Scholar using relevant keywords. Mechanistic, experimental, and clinical studies examining IL-4/IL-13 signaling and inhibitor outcomes were selected. IL-4 and IL-13 contribute to vascular inflammation by upregulating adhesion molecules, disrupting nitric oxide synthesis via arginase I, and increasing oxidative stress. These cytokines promote vascular remodeling and are linked to hypertension, atherosclerosis, and cardiac fibrosis. Inhibitors like dupilumab show promise in controlling inflammation, but their long-term cardiovascular effects remain unclear. Some studies suggest potential risks such as increased infections, metabolic dysregulation, and vascular stiffening. IL-4 and IL-13 are active mediators in cardiovascular pathology, offering both therapeutic potential and clinical challenges. While inhibitors targeting these cytokines may reduce inflammation, their broader impacts on vascular health warrant cautious and personalized application until long-term cardiovascular outcomes are clarified through further research.

Background: Atherosclerosis is a chronic, progressive vascular disease characterized not only by lipid accumulation but also by sustained inflammation. Recent evidence has highlighted the critical role of immune pathways and pro-inflammatory cytokines in plaque formation, progression, and destabilization. Aim: This narrative review aims to summarize current knowledge regarding the role of inflammation in atherosclerosis and evaluate the therapeutic potential of biologic agents targeting specific inflammatory pathways. Methods: A comprehensive literature search was conducted using keywords such as “atherosclerosis”, “inflammation”, “biologic agents”, and “cytokine inhibitors”. Recent clinical trials and relevant experimental studies were analyzed and synthesized narratively. Results: Biologic agents targeting IL-1β, IL-6, IL-17A, and CD20+ B cells have shown promising results in reducing inflammation and improving cardiovascular outcomes in high-risk patients. Agents such as canakinumab, anakinra, tocilizumab, rituximab, secukinumab, and alirocumab demonstrate varying degrees of efficacy depending on the targeted pathway. However, concerns remain regarding immunosuppression, lipid alterations, cost, and long-term safety. Conclusion: Biologic agents offer a novel, mechanism-based therapeutic approach in managing atherosclerosis. While current data support their benefit in select patient groups, further research is needed to clarify long-term outcomes, safety, and real-world applicability. Personalized treatment strategies based on inflammatory profiles may enhance clinical benefit.

Background: Systemic inflammation plays a central role in determining postoperative outcomes in patients undergoing isolated coronary artery bypass grafting with cardiopulmonary bypass. Traditional inflammatory indices such as the neutrophil-to-lymphocyte ratio and the platelet-to-lymphocyte ratio have prognostic value; however, their dynamic behavior during cardiopulmonary bypass remains insufficiently characterized. More comprehensive indices, including the systemic immune-inflammation index and the systemic inflammatory response index, may help characterize early intraoperative inflammatory activity; however, their prognostic relevance should be regarded as exploratory and requires prospective validation. Methods: This retrospective nested case–control study included 245 patients who underwent isolated coronary artery bypass grafting, and intraoperative inflammatory indices during cardiopulmonary bypass were evaluated. Because of the nested case–control design, mortality cases were intentionally overrepresented to improve statistical power; therefore, the observed mortality rate does not reflect the true institutional mortality rate. Inflammatory indices (NLR, PLR, SII, and SIRI) were calculated at induction, at the 5th, 45th, and 90th minutes during cardiopulmonary bypass, and in the early postoperative period. Associations between these indices and in-hospital mortality were evaluated using univariate and multivariable logistic regression analyses. Predictive performance was assessed using receiver operating characteristic (ROC) curve analysis and the area under the curve (AUC). Results: The final enriched analytical sample consisted of 51 mortality cases and 194 randomly sampled surviving controls. During cardiopulmonary bypass, inflammatory indices, particularly at the 5th minute, were significantly higher in patients who experienced mortality (p < 0.001 for all major indices). SII demonstrated the strongest predictive performance at the 5th minute (AUC = 0.790), followed by SIRI (AUC = 0.765), PLR (AUC = 0.687), and NLR (AUC = 0.681). In multivariable analysis, SII and SIRI measured at the 5th minute remained independent predictors of mortality. The addition of 5th-minute SII to the limited study-specific clinical model, which included age, ejection fraction, and preoperative creatinine, improved exploratory discrimination for in-hospital mortality (with AUC increasing from 0.698 to 0.797). Conclusions: Early intraoperative assessment of inflammatory indices during cardiopulmonary bypass may provide additional prognostic information in patients undergoing coronary artery bypass grafting. Composite indices, particularly SII and SIRI, showed stronger exploratory discrimination than traditional inflammatory markers in this enriched analytical sample. However, these findings should be considered hypothesis-generating and require prospective external validation before use in perioperative risk stratification or clinical decision-making can be recommended.

Dilated cardiomyopathy is characterized by progressive left ventricular dilation and impaired systolic function, with inflammation recognized as a key contributor to disease onset and adverse outcomes. C-reactive protein reflects systemic biochemical inflammation, whereas Delta Neutrophil Index represents the circulating immature neutrophil fraction and provides a cellular dimension of inflammatory burden. The combined diagnostic and prognostic value of these two biomarkers in dilated cardiomyopathy has not been adequately explored. This retrospective study included one hundred and fifty patients with dilated cardiomyopathy and one hundred and fifty age-, diabetes-, and hypertension-matched controls. Demographic, laboratory, and echocardiographic measurements were analyzed. The diagnostic and prognostic performances of C-reactive protein, Delta Neutrophil Index, and their combined model were assessed using logistic regression, receiver operating characteristic curve analysis, reclassification metrics, calibration testing, and decision curve analysis. Additional analyses were performed for patients with left ventricular ejection fraction below twenty percent, and mortality predictors were examined within the dilated cardiomyopathy cohort. Both C-reactive protein and Delta Neutrophil Index levels were significantly higher in patients with dilated cardiomyopathy than in controls and were further elevated in those with severely reduced ejection fraction. Delta Neutrophil Index remained independently associated with severe left ventricular dysfunction (ejection fraction ≤ 20%) in multivariable analysis (odds ratio 2.51). Each biomarker showed an independent association with the presence of dilated cardiomyopathy, and their combined model achieved the highest diagnostic accuracy. In receiver operating characteristic analysis, the area under the curve was 0.895 for Delta Neutrophil Index, 0.691 for C-reactive protein, and increased to 0.920 for the combined model, with a sensitivity of 81.3% and specificity of 92.0%. Delta Neutrophil Index was independently associated with severe left ventricular dysfunction and mortality, while C-reactive protein, age, ejection fraction, urea, and sodium also contributed to mortality risk. Delta Neutrophil Index was independently associated with mortality (odds ratio 2.51), while C-reactive protein, age, ejection fraction, urea, and sodium also contributed to mortality risk. The combined model provided significant improvement in risk reclassification and demonstrated superior calibration and greater net clinical benefit across a wide range of decision thresholds. C-reactive protein and Delta Neutrophil Index offer complementary diagnostic and prognostic information in dilated cardiomyopathy. Their combined use enhances diagnostic discrimination, strengthens risk stratification, and improves identification of patients at high risk for severe ventricular dysfunction and mortality. Incorporation of these accessible biomarkers into clinical evaluation may support earlier recognition and more tailored management of high-risk individuals.

Background: Inflammation plays a central role in the pathophysiology and clinical progression of acute myocardial infarction (MI). Although clopidogrel is known to exert potential anti-inflammatory effects in addition to platelet inhibition, the behavior of the early inflammatory response after treatment initiation and its prognostic significance remain unclear. This study aimed to evaluate dynamic inflammatory changes during the early post-treatment period and their association with in-hospital outcomes in patients with ST-elevation myocardial infarction. Methods: This retrospective, observational, single-center study included 300 patients with ST-elevation myocardial infarction treated with clopidogrel loading therapy. Systemic immune-inflammation index (SII), systemic inflammatory response index (SIRI), and delta neutrophil index (DNI) were evaluated before treatment and 24–48 h after therapy. In-hospital mortality and major adverse in-hospital outcomes were analyzed. Receiver operating characteristic analysis and multivariable logistic regression models were used to determine prognostic performance and independent predictors. Results: Contrary to the expected anti-inflammatory effect, all inflammatory markers significantly increased after clopidogrel therapy (all p < 0.05). Patients with persistent or increased inflammatory response demonstrated significantly higher rates of in-hospital mortality and major adverse outcomes. Post-treatment SIRI showed the strongest predictive performance for mortality (AUC: 0.81, 95% CI: 0.75–0.87), followed by ΔSIRI (AUC: 0.79). Multivariable analyses identified higher post-treatment inflammatory burden and dynamic inflammatory increases, particularly post-DNI and ΔSIRI, as independent predictors of mortality and adverse clinical course. Conclusions: Early inflammatory activation after clopidogrel therapy is strongly associated with poor in-hospital outcomes in patients with acute myocardial infarction. Persistent or increasing inflammatory burden may reflect an uncontrolled inflammatory response despite antiplatelet treatment and may serve as a practical and powerful prognostic marker for early risk stratification.

Venöz ve lenfatik sistem hastalıkları estetik kaygılara, şişliklere, ağrılara hatta venöz ülserlere sebep olarak kişinin yaşam kalitesini ciddi şekilde düşürebilir. Ayrıca ciddi maliyet ve iş gücü kaybına da neden olan hastalıklardandır. Venöz ve Lenfatik hastalıklarının tedavisi ülkemizde birçok merkezde yeni teknolojik cihazlar, ilaç pazarına yeni giren ilaçlar ve deneyim artışı ile başarılı bir şekilde gerçekleştirilmektedir. “Venöz ve Lenfatik Sistem Hastalıkları” adlı kitabımızı hazırlamamızdaki amacımız bu alanda çalışan tüm hekimlere güncel kılavuzlar eşliğinde pratik hayatta kullanabilecekleri faydalı bir kitap oluşturmaktı. Amacımızın gerçekleştiğini görmek bizi mutlu etti. Tüm çabalarımıza rağmen, gözden kaçırılan hatalardan dolayı okuyucularımızın hoşgörüsüne sığınıyoruz. Kitabın hazırlanmasında katkıda bulunan değerli meslektaşlarıma emekleri için çok teşekkür ediyorum.