Predictive Value of Apelin-36 for No-Reflow Phenomenon in STEMI Patients

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.