OBJECTIVE: To investigate vascular endothelial impairment as a result of reperfusion therapy in patients with acute myocardial infarction (AMI). METHODS: Patients with AMI underwent reperfusion therapy (percutaneous cardiac intervention [PCI] or thrombolytic therapy) or conservative drug therapy. Healthy control subjects were recruited. Endothelial impairment was assessed via endothelial nitric oxide (NO) synthase (eNOS), NO and endothelin-1 (ET-1) levels, 24 h after reperfusion or on enrolment, as appropriate. RESULTS: Patients who underwent PCI (n = 47) or thrombolytic therapy (n = 45) had significantly lower eNOS and NO levels, and higher ET-1 levels than those who received conservative drug therapy (n = 46). All patient groups had significantly lower eNOS and NO levels, and higher ET-1 levels, than controls (n = 45). There was a significant positive correlation between eNOS and NO, as well as significant negative correlations between eNOS/ET-1 and NO/ET-1 in all four groups. CONCLUSIONS: Patients with AMI who underwent reperfusion therapy displayed low eNOS activity. This may result in impairment of endothelial function via downregulation of NO and upregulation of ET-1.
OBJECTIVE: To investigate vascular endothelial impairment as a result of reperfusion therapy in patients with acute myocardial infarction (AMI). METHODS:Patients with AMI underwent reperfusion therapy (percutaneous cardiac intervention [PCI] or thrombolytic therapy) or conservative drug therapy. Healthy control subjects were recruited. Endothelial impairment was assessed via endothelial nitric oxide (NO) synthase (eNOS), NO and endothelin-1 (ET-1) levels, 24 h after reperfusion or on enrolment, as appropriate. RESULTS:Patients who underwent PCI (n = 47) or thrombolytic therapy (n = 45) had significantly lower eNOS and NO levels, and higher ET-1 levels than those who received conservative drug therapy (n = 46). All patient groups had significantly lower eNOS and NO levels, and higher ET-1 levels, than controls (n = 45). There was a significant positive correlation between eNOS and NO, as well as significant negative correlations between eNOS/ET-1 and NO/ET-1 in all four groups. CONCLUSIONS:Patients with AMI who underwent reperfusion therapy displayed low eNOS activity. This may result in impairment of endothelial function via downregulation of NO and upregulation of ET-1.