The effects of asymmetric dimethyl arginine and nitric oxide levels on early prognosis in patients with myocardial infarction
详细信息    查看全文
文摘

Objectives

It is unclear whether abnormalities of nitric oxide metabolism are related to hemodynamic dysfunction and mortality in patients with acute myocardial infarction (MI). Decreased nitric oxide (NOx) and high levels of asymmetric dimethyl arginine (ADMA) are proposed independent risk factors in coronary artery disease. We investigated the relationship of NOx and ADMA levels with early prognosis in patients with MI.

Design & Methods

59 patients (9 women and 50 men, aged 32–75) who were hospitalized at Coronary Care Unit and age-matched 20 healthy controls were included in the study. All clinical and laboratory parameters were monitored. Left ventricular systolic function (LVSF) was investigated by echocardiography as a prognostic marker of cardiac function. NO and ADMA levels were measured on the first day of infarction. NOx was measured spectrophotometrically at 430 nm using the Griess reaction with a commercial kit. Plasma ADMA concentrations were determined by competitive ELISA.

Results

MI patients had higher plasma ADMA (0,78  ± 0.44 μmol/L) levels than controls (0.45 ± 0.2 μmol/L). NOx levels were 35.6 ± 10.4 μmol/L in MI patients and 32.5 ± 3.7 μmol/L in controls. There was not a correlation between total and LDL-cholesterol, triglyceride, hs-CRP levels, smoking history, presence of hypertension or diabetes, localization and extent of infarction and ADMA and NOx levels.

Conclusion

MI patients had higher plasma ADMA levels than controls and there was not any relation with other coronary risk factors such as total and LDL-cholesterol, triglyceride, hs-CRP levels, smoking history, presence of hypertension or diabetes, localization and extent of infarction and ADMA and NOx levels. We also could not find a correlation between ADMA, NOx levels with LVSF and early cardiac events.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700