BACKGROUND: MicroRNA (miRNA) is reported to be present in human plasma and has been increasingly suggested as a biomarker for diseases. Our study aimed to investigate the kinetics of cardiac-specific microR-499 (miR-499) in acute myocardial infarction (AMI). METHODS: Circulating concentrations of cardiac enriched miR-499 were measured by quantitative PCR in 73 patients with acute coronary syndrome (ACS), including 53 with AMI and 20 with unstable angina (UA). Thirty healthy subjects were used as controls. Plasma samples in AMI group were obtained immediately after admission and at 12 h, 24 h, 3 d and 7 d after onset of symptoms. Plasma samples in UA and healthy control groups were collected immediately after admission. The severity and extent of coronary stenotic lesions were evaluated on the basis of coronary angiography using Gensini score. RESULTS: miR-499 expression levels were significantly higher in the 53 AMI patients than in the 20 UA patients and 30 healthy controls immediately after admission (P<0.01). A measurable increase in miR-499 levels was observed in AMI patients within 24 h of the last onset of chest pain and the levels returned to the baseline after 7 d. Plasma miR-499 levels in the patients with AMI were positively-correlated with cTnI (r=0.384, P<0.01) and CK-MB (r=0.402, P<0.01). In addition, miR-499 levels in AMI patients with two- and three-vessel coronary artery disease (CAD) were significantly higher than those in patients with single-vessel CAD (P<0.05). Gensini scores were used to evaluate the severity of coronary stenosis. miR-499 were positively correlated with Gensini scores (r=0.52, P<0.01). miR-499 levels at admission were significantly higher than that those 24 h after percutaneous coronary intervention (PCI) in AMI patients (P<0.01) and were negatively correlated with LVEF (r=0.36, P=0.008). CONCLUSIONS: Cardiac-specific miRNA-499 levels were found to be linearly proportional to myocardial damage. MiRNA-499 might prove to be a new biomarker for AMI and a predictor of the risk of myocardial ischemia.
BACKGROUND: MicroRNA (miRNA) is reported to be present in human plasma and has been increasingly suggested as a biomarker for diseases. Our study aimed to investigate the kinetics of cardiac-specific microR-499 (miR-499) in acute myocardial infarction (AMI). METHODS: Circulating concentrations of cardiac enriched miR-499 were measured by quantitative PCR in 73 patients with acute coronary syndrome (ACS), including 53 with AMI and 20 with unstable angina (UA). Thirty healthy subjects were used as controls. Plasma samples in AMI group were obtained immediately after admission and at 12 h, 24 h, 3 d and 7 d after onset of symptoms. Plasma samples in UA and healthy control groups were collected immediately after admission. The severity and extent of coronary stenotic lesions were evaluated on the basis of coronary angiography using Gensini score. RESULTS:miR-499 expression levels were significantly higher in the 53 AMI patients than in the 20 UA patients and 30 healthy controls immediately after admission (P<0.01). A measurable increase in miR-499 levels was observed in AMI patients within 24 h of the last onset of chest pain and the levels returned to the baseline after 7 d. Plasma miR-499 levels in the patients with AMI were positively-correlated with cTnI (r=0.384, P<0.01) and CK-MB (r=0.402, P<0.01). In addition, miR-499 levels in AMI patients with two- and three-vessel coronary artery disease (CAD) were significantly higher than those in patients with single-vessel CAD (P<0.05). Gensini scores were used to evaluate the severity of coronary stenosis. miR-499 were positively correlated with Gensini scores (r=0.52, P<0.01). miR-499 levels at admission were significantly higher than that those 24 h after percutaneous coronary intervention (PCI) in AMI patients (P<0.01) and were negatively correlated with LVEF (r=0.36, P=0.008). CONCLUSIONS: Cardiac-specific miRNA-499 levels were found to be linearly proportional to myocardial damage. MiRNA-499 might prove to be a new biomarker for AMI and a predictor of the risk of myocardial ischemia.
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