BACKGROUND: miR-23b overexpression can promote cardiomyocyte apoptosis and reduce cell growth under hypoxic conditions, suggesting that miR-23b acts as a biomarker for ST-elevation myocardial infarction (STEMI). The aim of this study was to investigate the effect of miR-23b on STEMI patients.

MATERIAL AND METHODS: We enrolled 80 eligible patients with STEMI and 60 control subjects. Blood samples were obtained at 6 h, 12 h, 24 h, 48 h, 3 days, and 7 days after the onset of symptoms. Another blood sample was collected before and after percutaneous coronary intervention (PCI). The samples were used for real-time quantitative PCR analysis. A Siemens Immulite2000 detector (Germany) was used for cTnI detection, and the serum CK-MB content was detected by electrochemical luminescence method.

RESULTS: The expression level of miR-23b was increased in patients with STEMI (P<0.05). No significance difference was observed among risk factors, although the clinical data was comparable (P>0.05). The level of miR-23b in STEMI patients after PCI was lower (P<0.05). The ROC curve of plasma miR-23b showed a separation, with an AUC of 0.809 (95%CI, 0.737–0.936, P<0.05), compared to CK-MB with an AUC of 0.753 (95%CI, 0.707–0.896) and cTnI with an AUC of 0.783 (95%CI, 0.723–0.917).

CONCLUSIONS: The present study reveals that miR-23b is a useful biomarker of STEMI, providing a novel insight for the diagnosis for STEMI.

Keywords: Anterior Wall Myocardial Infarction, Creatine Kinase, MB Form, troponin I