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: 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: 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.