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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
Serum nitric oxide levels in patients with coronary artery ectasia
Adalet Gürlek1, Kerim Esenboğa2, Özgür Ulaş Özcan1
1Department of Cardiology, Faculty of Medicine, Ankara University, Ankara-Turkey.
Insights
This study found significantly lower serum nitric oxide (NO) levels in patients with coronary artery ectasia (CAE). These findings suggest that reduced NO may contribute to the development of CAE.
Area of Science:
- Cardiology
- Biochemistry
Background:
- Atherosclerosis is linked to decreased nitric oxide (NO) levels.
- Endothelial dysfunction and atherosclerosis are potential causes of coronary artery ectasia (CAE).
Purpose of the Study:
- To investigate the relationship between serum NO levels and CAE.
- To determine if NO levels are a risk factor for CAE development.
Main Methods:
- A prospective controlled study compared 40 CAE patients with 40 controls.
- Serum NO levels were measured and analyzed using logistic regression and ROC curves.
- Exclusion criteria included stenotic plaques, slow flow, prior revascularization, acute coronary syndromes, and other cardiovascular conditions.
Main Results:
- Serum NO concentrations were significantly lower in CAE patients (42.1±20.1 µmol/L) versus controls (77.3±15.7 µmol/L).
- Low NO levels (OR=0.88) and LDL levels were independent factors associated with CAE.
- A NO cut-off of 63.3 µmol/L predicted CAE with 87.5% sensitivity and 90% specificity.
Conclusions:
- Decreased serum NO levels are associated with CAE.
- This supports the hypothesis that reduced NO contributes to the pathogenesis of CAE.
Objective:
Serum levels of nitric oxide (NO) are decreased in patients with atherosclerosis and also are a risk factor for the development of atherosclerosis. Endothelial dysfunction and diffuse atherosclerosis have been proposed for the etiology of coronary artery ectasia (CAE). The purpose of this clinical trial was to determine the relationship between CAE and serum NO levels.
Methods:
This prospective controlled study was conducted between January 2008 and March 2012. Serum levels of NO were compared in 40 patients with CAE (mean age 60.1±7.3 years) and 40 patients with normal coronary arteries (mean age 57.6±5 years) as a control group. CAE was diagnosed when a segment of coronary artery was more than 1.5 times the diameter of the adjacent healthy segment. Patients with stenotic atherosclerotic plaques, slow coronary flow, previous history of revascularization, acute coronary syndromes, left ventricular dysfunction, valvular heart disease, and systemic diseases were not included in the study. The effect of NO on the outcome was studied by constructing a receiver operating characteristic (ROC) curve with CAE as the primary variable. Effects of different variables on CAE were calculated using binary logistics regression analysis.
Results:
Serum NO concentrations were significantly lower in patients with CAE than in the control group (42.1±20.1 µmol/L vs. 77.3±15.7 µmol/L, p<0.001). According to the results of the multivariate regression analysis, LDL and NO levels were identified as independent factors associated with CAE (OR=1.02, 95% CI 1-1.04, p=0.02 and OR=0.88, 95% CI 0.83-0.93, p=0.001, respectively). ROC analysis revealed that using a cut-off point of 63.3, NO level predicts CAE with a sensitivity of 87.5% and specificity of 90%.
Conclusion:
Our study indicates that decreased levels of NO are present in patients with CAE compared to patients with normal coronary arteries, supporting the hypothesis that decreased levels of NO might be associated with CAE development.
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