OBJECTIVE: To examine the expression of circulating microRNA-92a (miR-92a) in patients with ST-segment elevation myocardial infarction (STEMI), and the impact of percutaneous coronary intervention (PCI) on such expression. METHODS: The level of circulating miR-92a was measured in three groups of patients: 58 STEMI patients received PCI, 24 STEMI patients received no PCI, and 116 patients with stable angina pectoris (SAP) without PCI. RESULTS: On the day next to admission, STEMI patients received no PCI were found to have higher level of circulating miR-92a as compared to SAP patients without PCI (0.2869 ± 0.8167 vs. -0.0555 ± 0.9855, F = 2.438, P = 0.121). Twenty-four hours after the PCI, the level of circulating miR-92a in STEMI patients received the procedure was lower than those without it (-0.0324 ± 0.9563 vs. 0.2869 ± 0.8167, F = 2.054, P = 0.156). The SAP patients (without PCI) had higher survival rate as compared to the STEMI patients without PCI (100.0% vs. 75.0% P = 0.001), and the survival rate in STEMI patients received PCI was higher than those without it (89.7% vs. 75.0%, P = 0.088). CONCLUSIONS: In STEMI patients, the expression of circulating miR-92a is up-regulated. PCI therapy may suppress such up-regulation. Survival rate is higher in patients showing down-regulation of miR-92a. Our data suggest that miR-92a might have potential for diagnosis and therapeutic application in the prevention and treatment of STEMI.
OBJECTIVE: To examine the expression of circulating microRNA-92a (miR-92a) in patients with ST-segment elevation myocardial infarction (STEMI), and the impact of percutaneous coronary intervention (PCI) on such expression. METHODS: The level of circulating miR-92a was measured in three groups of patients: 58 STEMI patients received PCI, 24 STEMI patients received no PCI, and 116 patients with stable angina pectoris (SAP) without PCI. RESULTS: On the day next to admission, STEMI patients received no PCI were found to have higher level of circulating miR-92a as compared to SAP patients without PCI (0.2869 ± 0.8167 vs. -0.0555 ± 0.9855, F = 2.438, P = 0.121). Twenty-four hours after the PCI, the level of circulating miR-92a in STEMI patients received the procedure was lower than those without it (-0.0324 ± 0.9563 vs. 0.2869 ± 0.8167, F = 2.054, P = 0.156). The SAP patients (without PCI) had higher survival rate as compared to the STEMI patients without PCI (100.0% vs. 75.0% P = 0.001), and the survival rate in STEMI patients received PCI was higher than those without it (89.7% vs. 75.0%, P = 0.088). CONCLUSIONS: In STEMI patients, the expression of circulating miR-92a is up-regulated. PCI therapy may suppress such up-regulation. Survival rate is higher in patients showing down-regulation of miR-92a. Our data suggest that miR-92a might have potential for diagnosis and therapeutic application in the prevention and treatment of STEMI.