Open AccessImpairment of vascular endothelial function following reperfusion therapy in patients with acute myocardial infarction
Author(s) -
Zhaoying Yang,
Jinliang Li,
Jing Kong,
WU Sui-sheng
Publication year - 2013
Publication title -
journal of international medical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.421
H-Index - 57
eISSN - 1473-2300
pISSN - 0300-0605
DOI - 10.1177/0300060513487650
Subject(s) - medicine , enos , cardiology , reperfusion therapy , conventional pci , myocardial infarction , percutaneous coronary intervention , endothelial dysfunction , endothelin 1 , nitric oxide , endothelin receptor , nitric oxide synthase , receptor
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.