Background: Dipeptidyl peptidase 3 (DPP-3) is an intracellular enzyme that causes hemodynamic instability and cardiac depression in several cases such as cardiogenic shock, sepsis and burns where DPP-3 is released into the blood due to cell death. Data on the effect of higher DPP-3 levels on acute coronary syndrome (ACS) patients are currently lacking. The aim of this study was to evaluate the effect of DPP-3 levels on ACS patients. Methods: In this prospective study, we included ACS patients including STEMI and non-STEMI groups and a control group to compare various demographic, echocardiographic and laboratory parameters including DPP-3. DPP-3 levels were measured at 24^th, 48^th, and 72^nd h from the onset of symptoms in ACS patients and then compared with left ventricle ejection fraction (LVEF) for the assessment of left ventricle systolic function. Results: A total of 70 ACS patients (age 62.5 ± 11 years, 68.6% male) were recruited and 48 normal individuals were included as control group (age 61.1 ± 10 years, 66.7% male). It has been demonstrated that DPP-3 levels are significantly higher in the ACS group than the control group like troponin I levels. DPP-3 levels were found to be one of the independent predictors of LVEF similar to NT-proBNP and troponin I. Conclusions: This study suggests that DPP-3 could be an important indicator of myocardial depression predicting left ventricle systolic function in ACS.

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: 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.

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.

Akut koroner sendromlarda (miyokard infarktüsü, kararsız angina) intrakoroner trombüs görülme oranı yüksektir. Miyokard infaktüsü ile gelen hastalarda intrakoroner trombüs mevcudiyeti güncel müdahale tekniklerine rağmen işlem başarısını düşürmekte ve çeşitli komplikasyonlara neden olmaktadır. Bizim vakamızda 49 yaşında erkek hastada gelişen komplikasyonlar ve yönetimi sunulmuştur. ST elevasyonlu miyokard infarktüsü ile gelen hastanın son ön inen koroner arterde trombüsün aspirasyonu sonrası tüm sol sistemde yaygın trombüs gözlemlendi. İntrakoroner heparin ve tirofiban sonrasında trombüs geriledi ve direkt stent implantasyonu ile kompikasyon başarılı bir şekilde yönetildi. Son kılavuzlarda da gösterildiği üzere trombüs aspirasyonu, yoğun koroner arter trombüsü olması durumunda mortaliteyi istatistiksel olarak anlamlı olmasa da azalttığı gösterilmiş ancak koroner arter trombüs aspirasyonu rutin olarak önerilmemektedir.

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.