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.

Early in-hospital mortality remains an important concern after coronary artery bypass grafting. Existing risk scores, such as EuroSCORE and STS, rely mainly on demographic and clinical parameters and do not adequately incorporate routine hematological markers. This study aimed to develop and validate the Hematological Inflammatory Gradient Score (HIGS), a novel model derived from routinely available hematological indices, to predict early postoperative mortality after coronary artery bypass grafting (CABG). A retrospective, single-center cohort of 202 patients undergoing elective isolated CABG between January 2022 and March 2024 was analyzed. HIGS was calculated using standardized z-scores of red cell distribution width (RDW), platelet distribution width (PDW), and immature granulocyte percentage (IG%). Discrimination was assessed with ROC curve analysis, while logistic regression identified independent predictors of mortality. In-hospital mortality occurred in 10.9% (22/202) of patients. Compared with survivors, non-survivors had significantly higher HIGS values (1.02 ± 0.74 vs –0.12 ± 0.43, p < 0.001). HIGS demonstrated the highest discriminative ability for mortality prediction among tested parameters (AUC = 0.862, 95% CI: 0.794–0.931), with 86.4% sensitivity and 78.9% specificity at the optimal cut-off (>0.44). When added to the base model consisting of age, ejection fraction, and urea, HIGS provided a modest improvement in discrimination (AUC increase from 0.639 to 0.665). In multivariate analysis, lower ejection fraction, higher IG%, and elevated urea were independent predictors of mortality, and inclusion of HIGS improved model performance. HIGS is a simple, inexpensive, and biologically plausible score derived from routine blood tests that reliably stratifies early mortality risk after CABG. If confirmed in larger, prospective multicenter studies, HIGS may serve as a practical adjunct to conventional risk models in perioperative decision-making. Given the retrospective, single-center design and limited event count, these findings should be interpreted cautiously, and external validation is required.

Background: Coronary anatomical complexity is commonly used for perioperative risk assessment in patients undergoing coronary artery bypass grafting (CABG), although it may not fully reflect systemic biological vulnerability. This study aimed to evaluate the association between the Prognostic Nutritional Index (PNI), a nutritional–immune marker derived from serum albumin and lymphocyte counts, and in-hospital mortality after CABG in relation to coronary anatomical complexity and established surgical risk scores. Methods: In this single-center retrospective cohort study, 324 consecutive patients who underwent isolated CABG between April 2024 and April 2025 were analyzed. The PNI was calculated according to the standard Onodera formula using preoperative serum albumin and total lymphocyte count. Associations with in-hospital mortality were evaluated using univariable and multivariable logistic regression analyses. Discriminative performance was assessed using receiver operating characteristic curve analysis, while exploratory analyses evaluating the additional prognostic contribution of the PNI beyond surgical risk scores were performed using nested model comparison and reclassification analyses. Internal validation and calibration analyses were also performed. Results: In-hospital mortality occurred in 26 patients. Preoperative and postoperative PNI values were significantly lower in patients who experienced in-hospital mortality. In multivariable analysis, the postoperative PNI remained independently associated with in-hospital mortality, whereas the preoperative PNI lost statistical significance after adjustment for clinical, renal, and surgical risk parameters. Receiver operating characteristic analysis demonstrated modest discriminative ability for the preoperative PNI (AUC: 0.742, 95% CI: 0.661–0.823). Exploratory analyses suggested a modest improvement in model discrimination and risk classification after the addition of the PNI to STS-based models; however, the overall incremental prognostic contribution remained limited. Calibration and internal validation analyses demonstrated acceptable agreement between predicted and observed mortality risk. Conclusions: The postoperative PNI demonstrated a stronger and independent association with in-hospital mortality than the preoperative PNI, suggesting that early postoperative nutritional–immune deterioration may reflect the magnitude of perioperative physiological stress and evolving clinical deterioration after CABG. Although lower preoperative PNI values were associated with mortality in univariable analyses, this association was no longer statistically significant after adjustment for clinical, renal, and surgical risk parameters. These findings indicate that postoperative nutritional–immune status may provide complementary biological information beyond conventional risk models; however, its clinical utility requires confirmation in larger prospective multicenter studies.

Background: The C-reactive protein-to-albumin ratio (CAR) has emerged as a composite biomarker reflecting both systemic inflammation and nutritional status. This study investigated the prognostic value of preoperative and postoperative CAR in predicting early mortality following coronary artery bypass grafting (CABG). Methods: This retrospective study included 273 patients who underwent isolated CABG. Patients were categorized as mortality (+) (Ex group, n = 41) and mortality (−) (Non-Ex group, n = 232). Preoperative and postoperative CAR values were calculated and compared between groups. Independent predictors of mortality were evaluated using logistic regression analysis. Discriminative performance was assessed using receiver operating characteristic (ROC) curve analysis. Results: Early mortality occurred in 41 patients (15.0%). Both preoperative and postoperative CAR values were significantly higher in the mortality (+) group compared with the mortality (−) group. In multivariable logistic regression analysis, postoperative creatinine remained independently associated with early mortality, whereas neither preoperative nor postoperative CAR retained independent statistical significance after adjustment for clinical variables and renal function despite moderate discriminative performance in crude and ROC-based analyses. ROC analysis showed that CAR demonstrated moderate discriminative ability for mortality prediction, with postoperative CAR showing better performance than preoperative CAR. Conclusions: Although CAR demonstrated moderate discriminative performance for early mortality after CABG in unadjusted analyses, it did not independently predict mortality after adjustment for clinical variables and renal function. Therefore, CAR may be more appropriately interpreted as a supportive inflammation-based risk stratification marker rather than a stand-alone prognostic predictor.

Postoperative depression and anxiety are common psychological conditions following cardiac surgery, often underestimated despite their significant impact on recovery. These disorders hinder physical healing, complicate rehabilitation, and reduce quality of life. Despite their prevalence, they are frequently overlooked in clinical settings. This study aims to explore the psychological burden after cardiac surgery, focusing on postoperative depression and anxiety. It examines the prevalence of these disorders, identifies contributing risk factors, and evaluates management strategies. A narrative review of the existing literature is conducted, synthesizing studies on postoperative depression and anxiety in cardiac surgery patients. The review investigates demographic, medical, surgical, psychosocial, and recovery-related factors that contribute to the onset of these psychological issues. Additionally, it assesses treatment effectiveness, including pharmacotherapy, psychotherapy, and psychoeducation. Postoperative depression and anxiety affect 20-30% of patients after cardiac surgery. Key risk factors include age, gender, socioeconomic status, psychiatric history, and the severity of heart disease. The effectiveness of antidepressants, anxiolytics, cognitive-behavioral therapy (CBT), and cardiac rehabilitation in improving symptoms and aiding recovery is also discussed. Addressing these psychological conditions is crucial for optimizing both psychological and physical recovery in cardiac surgery patients. A multidisciplinary approach, combining psychological support with traditional medical treatment, is vital for improving patient outcomes.