Background: A decreased level of adiponectin is known as a predictor of adverse left ventricular remodeling and major adverse cardiac events (MACEs). We evaluated long-term MACEs following ST-segment elevation myocardial infarction (STEMI) in relation to adiponectin levels. Methods: This prospective study included a total of 73 consecutive STEMI patients. Adiponectin, CK, CK-MB, cTnI, CRP, HDL cholesterol, LDL cholesterol, triglycerides, and other routine laboratory parameters were considered, and myocardial revascularization and two-dimensional echocardiography were performed. Subjects were divided into two groups according to their serum adiponectin concentrations. Results: In total, 24 (32.87%) patients suffered from MACEs, 19 (26.02%) with adiponectin value ≤ 1.8 ng/mL (group 1) and 5 (6.84%) with adiponectin value > 1.8 ng/mL (group 2) (p < 0.013). Heart failure (Killip >1) was present in 14 cases (19.17%) in group 1 and in 3 cases (4.1%) in group 2 (p < 0.001). Kaplan–Meier analysis was used to depict the occurrence of MACEs according to the adiponectin threshold identified during hospitalization (1.8 ng/mL). The log-rank test revealed a statistically significant difference in survival between groups (p = 0.013), and the AUC value for adiponectin was 0.77 (95% CI, 0.66–0.89), p = 0.01. Based on univariate logistic regression analysis, adiponectin and BMI were significantly associated with MACEs (p = 0.018, p = 0.034). Multivariate logistic regression analysis shows that serum adiponectin predicts MACEs after STEMI (p = 0.011). Conclusions: We found significant associations between adiponectin levels and MACEs in patients who survived STEMI. The established cut-off value of 1.8 ng/mL for adiponectin during hospitalization identified patients at risk for MACEs.

Background: Apelin-36 may be used to identify patients with ST-segment elevation myocardial infarction (STEMI) who are at risk for the no-reflow phenomenon. Patients presenting with STEMI were evaluated and stratified according to their apelin-36 levels. Methods: In this study, 161 patients presenting with STEMI within 12 hours of symptom onset and undergoing primary percutaneous coronary intervention (pPCI) were enrolled. Biochemical parameters, including apelin-36, troponin T, creatine kinase (CK), the MB fraction of creatine kinase (CK-MB), total cholesterol, triglycerides, and other routine laboratory parameters, were measured. Blood samples for apelin-36 measurement were collected prior to PCI, centrifuged to obtain serum, and preserved at -80⁰C until being assayed. Two-dimensional echocardiography was performed in all patients. Thereafter, patients were divided into two groups according to their level of Apelin-36. Results: Among the 161 consecutive STEMI patients, 115 (71.42%) had Apelin-36 levels ≤0.58ng/mL (group 1), whereas 46 (28.57%) had Apelin-36 levels > 0.58ng/mL (group 2). In total, 51 (31.67%) STEMI patients experienced no-reflow phenomenon after PCI: 29 (18.01%) patients with apelin-36 ≤ 0.58ng/mL and 22 (13.66%) with a value > 0.58ng/mL (p < 0.001). In terms of Gensini score, the mean value in group 1 was (70.29 (±28.76), while in group 2, it was 81.95 (±23.82) (p=0.004). Overall, a positive correlation between apelin-36 and Gensini score was observed in both groups using Kendall’s correlation analysis (group 1: Figure 2, p=0.05; group 2: Figure 2, p 0.58ng/mL had troponin T levels of 132.15 (9.4-5190.0) (p < 0.012). The receiver operating characteristics (ROC) curve of apelin-36 was used to plot the true positive rate against the false positive rate at different cut-off points, with AUC=0.67 (95% CI, 0.57-0.76), and the cut-off value for apelin-36 was 0.58ng/mL, with p=0.001. Conclusions: Significant associations were observed between apelin-36 and no-reflow phenomenon in patients with STEMI. An apelin-36 cut-off value of 0.58ng/mL, measured at admission, could be used to identify patients who were at increased risk of no-reflow phenomenon/reperfusion injury.

Background: In patients with ST-segment elevation myocardial infarction (STEMI), apelin is upregulated and exerts cardioprotective effects against ischemia–reperfusion injury (IRI). The present study aimed to investigate serum apelin-36 levels in STEMI patients and their relationship with the no-reflow phenomenon. Methods: In this study, 161 patients presenting with STEMI within 12 h of symptom onset and undergoing primary percutaneous coronary intervention (pPCI) were enrolled. Biochemical parameters, including apelin-36, troponin T, creatine kinase (CK), the MB fraction of creatine kinase (CK-MB), total cholesterol, triglycerides, and other routine laboratory parameters, were measured. Two-dimensional echocardiography was performed in all patients. Thereafter, patients were divided into two groups according to their level of aaapelin-36. Results: Among the 161 consecutive STEMI patients, 115 (71.42%) had Apelin-36 levels ≤ 0.58 ng/mL (group 1), whereas 46 (28.57%) had Apelin-36 levels > 0.58 ng/mL (group 2). In total, 51 (31.67%) STEMI patients experienced no-reflow phenomenon after PCI: 29 (25.21%) of patients with apelin-36 ≤ 0.58 ng/mL and 22 (47.82%) of those with a value > 0.58 ng/mL (p < 0.001). In terms of Gensini score, the mean value in group 1 was 70.29 (±28.76), while in group 2, it was 81.95 (±23.82) (p = 0.004). Overall, a positive correlation between apelin-36 and Gensini score was observed in both groups using Kendall’s correlation analysis (group 1: p = 0.05; group 2: p < 0.0001). Binary logistic regression analysis identified apelin-36 and diabetes mellitus as significant predictors at the 5% level, with p-values of 0.045 and 0.036, respectively. Patients with apelin-36 levels ≤ 0.58 ng/mL had troponin T levels of 290.0 (8.5–9510.0), while those with a value > 0.58 ng/mL had troponin T levels of 132.15 (9.4–5190.0) (p < 0.012). The receiver operating characteristics (ROC) curve of apelin-36 was used to plot the true positive rate against the false positive rate at different cut-off points, with AUC = 0.77 (95% CI, 0.69–0.84), and the cut-off value for apelin-36 was 0.58 ng/mL, with p = 0.001. Conclusions: Significant associations were observed between apelin-36 and the no-reflow phenomenon in patients with STEMI. An apelin-36 cut-off value of 0.58 ng/mL, measured at admission, could be used to identify patients who were at increased risk of no-reflow phenomenon/reperfusion injury.

Background: The C-reactive protein/albumin ratio (CAR) has increasingly attracted attention as a reliable predictive marker in patients with acute myocardial infarction (AMI). Purpose: This study aimed to evaluate the predictive value of the CAR for no-reflow development. Methods: A total of 201 patients with STEMI who underwent PCI were included in the study. Admission laboratory tests included CRP, albumin, CK, CK-MB, troponin T, and other biochemical parameters. The CAR was calculated as CRP divided by albumin ×100, while the CUAR was calculated as the base-10 logarithm of CRP × UA divided by albumin. Patients were then divided into two groups based on CAR levels. Results: A total of 201 STEMI patients were included: 106 (52.7%) in the low-CAR group (≤48.4) and 95 (47.3%) in the high-CAR group (>48.4). Significant differences between groups were observed for smoking, albumin, cholesterol, CRP, CUAR, and TIMI flow grade ≤ 2. Logistic regression analysis identified albumin, cholesterol, CRP, BUN, uric acid, CK-MB, CAR, and CUAR as significant predictors of TIMI flow grade. A receiver operating characteristic (ROC) curve of CRP, albumin, CAR, and CUAR was used to plot the true positive rate against the false positive rate across various cut-off points; the area under the curve (AUC) was 0.87 (95% CI, 0.81–0.94, p < 0.0001) for CRP, 0.73 (95% CI, 0.65–0.81, p < 0.0001) for albumin, 0.9 (95% CI, 0.84–0.95, p < 0.0001) for the CAR, and 0.94 (95%, 0.89–0.99, p < 0.0001) for the CUAR. The cut-off values were 2.11 for the CUAR, 48.4 for the CAR, 18 for CRP, and 38 for albumin. Conclusions: The ratio of C-reactive protein to albumin (CAR) may serve as a reliable and clinically accessible marker associated with the no-reflow phenomenon in STEMI patients undergoing PCI. A defined CAR cut-off has been proposed to help stratify patients at increased risk of no-reflow.

Background and Objectives: The coexistence of elevated hs-CRP levels and diabetes mellitus may play an important role in plaque destabilization, favoring plaque rupture and thrombosis, and consequently increasing the risk of coronary artery occlusion and acute coronary syndrome. In this study, we aimed to assess the association of the CRP–glycemia index with coronary artery occlusion at presentation in diabetic patients with ST-segment elevation myocardial infarction (STEMI) and evaluate its potential role as a marker of angiographically confirmed total occlusion. Materials and Methods: In total, 131 consecutive patients presenting with ST-segment elevation myocardial infarction (STEMI) within 12 h of symptom onset who underwent percutaneous coronary intervention (PCI) were included in this study. At patient admission, laboratory assessments were performed, including creatine kinase (CK), CK-MB, troponin I, high-sensitivity C-reactive protein (hs-CRP), glucose, blood urea nitrogen (BUN), creatinine, cholesterol, and standard biochemical parameters. The hs-CRP–glycemia index (CRPGI) was calculated using the following formula: CRPGI = CRP (mg/L) × glucose (mmol/L). Based on the presence of coronary artery occlusion, patients were stratified into two groups: those with acute coronary syndrome and total coronary artery occlusion (ACS/CA–total occlusion (TO), Group 1) and those with ACS and non-total coronary artery occlusion (ACS/CA–non-total occlusion (nTO), Group 2). Results: Of the 131 diabetic patients with STEMI who were treated with PCI, 77 (58.78%) had ACS/CA-TO (Group 1), while 54 (41.22%) had ACS/CA-nTO (Group 2). The CRPGI differed significantly between the groups, p < 0.0001. Significant differences were also observed in glucose, hs-CRP levels, CK, CK-MB, troponin I, and ejection fraction (EF) (p = 0.011, p < 0.0001, p < 0.0001, p < 0.0001, p = 0.004, and p < 0.0001, respectively). Based on binary logistic regression analysis, glucose, and hs-CRP were significantly associated with coronary occlusion, with ORs of 1.115 (p = 0.027), and 1.114 (p < 0.0001), respectively. In the model incorporating the CRPGI, this index was also significantly associated with coronary occlusion (OR, 1.001; 95% CI, 1.000–1.001; p < 0.006). ROC analysis demonstrated the good discriminatory ability of CRPGI, with an AUC of 0.87 (95% CI, 0.80–0.93) and an exploratory optimal threshold of 201.49 (p < 0.0001). Conclusions: The hs-CRP–glycemia index (CRPGI) is associated with angiographically confirmed total coronary artery occlusion in diabetic patients with STEMI, and it may represent a clinically relevant marker accompanying and potentially reflecting the extent of coronary occlusion at the time of presentation.

Background: The coexistence of elevated hs-CRP levels and diabetes mellitus may play a significant role in plaque destabilization, favoring plaque rupture and thrombosis, and consequently increasing the risk of coronary artery occlusion and acute coronary syndrome. Purpose: This study aimed to assess the CRP-glycemia index as potential predictors of of coronary artery occlusion in diabetic patients with acute coronary syndrome. Methods: The study included 131 consecutive patients presenting with ST-segment elevation myocardial infarction (STEMI) within 12 hours of symptom onset who underwent percutaneous coronary intervention (PCI). At admission, laboratory assessments were performed, including creatine kinase (CK), CK-MB, troponin I, high-sensitivity C-reactive protein (hs-CRP), glucose, blood urea nitrogen (BUN), creatinine, cholesterol, and standard biochemical parameters. The CRP–glycemia index (CRPGI) was calculated using the formula: CRPGI = CRP (mg/L) × glucose (mmol/L). Based on the presence of coronary artery occlusion, patients were stratified into two groups: those with acute coronary syndrome and total coronary artery occlusion (ACS/CA-total occlusion (TO), Group 1) and those with ACS and non-total coronary artery occlusion (ACS/CA-non-total occlusion (nTO), Group 2). Results: Of the 131 diabetic patients with STEMI treated with PCI, 77 (58.77) had ACS/CA-TO (Group 1), while 54 (41.22%) had ACS/CA-nTO (Group 2) (Table 1). CRPGI differed significantly between the groups, p<0.0001. Significant differences were also observed in glucose, hs-CRP levels, CK, CK-MB, troponin I, and ejection fraction (EF) (p=0.011, p<0.0001, p<0.0001, p<0.000, p=0.004 and p<0.0001, respectively). Based on binary logistic regression, we analyzed the relationship between one dichotomous dependent variable (ACS/CA-TO or ACS/CA-nTO) and other variables (age hypertension, BMI, diabetes mellitus, smoking, glucose, hs-CRP, and CRP–glycemia index (CRPGI). Glucose, hs-CRP, and CRPGI are significant predictors at the 5% level, with p-values of 0.007, <0.0001 and <0.0001 respectively (Table 2). The ROC analysis of the CRPGI demonstrates an AUC of 0.87 (95% CI: 0.80–0.93), with an optimal threshold of 201.49 (p < 0.0001) (Table 3). Table 3 further summarizes the AUCs for the other biomarkers included in the study. Figure 1 presents the ROC curve analyses for the studied biomarkers, showing a progressive increase in predictive significance from glucose to CRP and finally to the CRP–glycemia index (CRPGI). Conclusions: The CRP–glycemia index (CRPGI) appears to be a valuable predictor of coronary artery occlusion in diabetic patients with STEMI, highlighting its potential utility for risk stratification and early clinical assessment.