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Updated: Jul 17, 2026

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
Published on: April 27, 2016
Effect of homocysteine-induced oxidative stress on endothelial function in coronary slow-flow
Halil Tanriverdi1, Harun Evrengul, Yasar Enli
1Department of Cardiology, Pamukkale University School of Medicine, Denizli, Turkey. htanriverdi@pau.edu.tr
Insights
Patients with coronary slow-flow (CSF) phenomenon exhibit elevated plasma homocysteine (Hcy) levels and increased oxidative stress. These factors are linked to impaired endothelial function, a key finding in CSF.
Area of Science:
- Cardiology
- Vascular Biology
- Biochemistry
Background:
- Coronary slow-flow (CSF) phenomenon involves delayed coronary artery opacification without obstructive lesions.
- The exact cause of CSF is unknown, but endothelial dysfunction and elevated homocysteine (Hcy) are suspected contributors.
- Oxidative stress may play a role in the pathogenesis of CSF.
Purpose of the Study:
- To investigate endothelial function in patients with CSF.
- To examine the relationship between Hcy levels, oxidative stress markers, and endothelial function in CSF patients.
- To compare these parameters between CSF patients and healthy controls.
Main Methods:
- 44 patients with angiographically confirmed CSF and 44 controls were studied.
- Coronary flow was assessed using the TIMI frame count.
- Endothelial function was evaluated via flow-mediated dilation (FMD) using high-frequency ultrasound.
- Blood samples were analyzed for homocysteine (Hcy), superoxide dismutase (SOD), reduced glutathione (GSH), and malondialdehyde (MDA).
Main Results:
- CSF patients had significantly higher plasma Hcy levels (12.2 ± 4.9 vs. 8.5 ± 2.8 μmol/l, p=0.0001).
- Endothelial-dependent FMD was significantly reduced in CSF patients (4.98 ± 1.1% vs. 7.87 ± 2.0%, p=0.0001).
- CSF patients showed reduced GSH and elevated SOD and MDA, indicating increased oxidative stress.
- Plasma Hcy positively correlated with TIMI frame count and negatively with FMD.
Conclusions:
- Patients with CSF demonstrate elevated Hcy levels and markers of oxidative stress.
- Impaired endothelial cell function is a significant finding in individuals with CSF.
- Hcy and oxidative stress are implicated in the pathophysiology of the coronary slow-flow phenomenon.
Background And Objective:
Coronary slow-flow (CSF) phenomenon is characterized by delayed opacification of vessels in a normal coronary angiogram, but its etiopathogenesis remains unclear. Plasma homocysteine (Hcy) level can severely disturb vascular endothelial function and may play a role in the pathogenesis of CSF. In our study, endothelial function in patients with CSF and their relationship with Hcy and oxidative stress parameters are investigated.
Method:
Forty-four patients with angiographically proven CSF and 44 cases with normal coronary flow pattern with similar risk profile were enrolled in the study. Coronary flow patterns of the cases are determined by Thrombolysis in Myocardial Infarction (TIMI) frame count method. Endothelium dependent flow mediated dilatation (FMD) and independent vasodilatation characteristics are evaluated by high frequency ultrasound over the brachial artery. Superoxide dismutase (SOD) and reduced glutathione (GSH) and reduction of oxidative material in the body and the end product of lipid peroxidation, malondialdehyde (MDA) are measured as oxidative stress markers in blood samples.
Results:
Plasma Hcy level (micromol/l) of patients with CSF was found to be significantly higher than in controls (12.2 +/- 4.9 vs. 8.5 +/- 2.8, p = 0.0001). FMD was 7.87 +/- 2.0% in controls and 4.98 +/- 1.1% in patients with CSF (p = 0.0001). GSH was reduced in patients with CSF. SOD and MDA activity were found higher in patients with CSF than control subjects. Plasma Hcy level was significantly positively correlated with mean TIMI frame count and negatively correlated with FMD in correlation analysis (r = 0.58, p = 0.0001; r = -0.41, p = 0.022; respectively).
Conclusion:
The present findings allow us to conclude that patients with CSF have increased levels of Hcy and oxidative stress markers and impaired endothelial cell function.
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