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Updated: Jun 5, 2026

Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
Published on: October 22, 2014
The effects of endothelial dysfunction and inflammation on slow coronary flow
Hasan Arı1, Selma Arı, Ercan Erdoğan
1Department of Cardiology, Bursa Yüksek İhtisas Heart-Education and Research Hospital, Bursa, Turkey. hasanari03@yahoo.com
Insights
Endothelial dysfunction, indicated by elevated asymmetric dimethylarginine (ADMA) and reduced flow-mediated dilatation (FMD), is linked to slow coronary flow (SCF). Inflammation does not appear to be a significant factor in SCF development.
Area of Science:
- Cardiology
- Vascular Biology
- Biomedical Research
Background:
- Slow coronary flow (SCF) is a condition affecting coronary artery blood flow.
- The underlying mechanisms of SCF, particularly the roles of endothelial dysfunction and inflammation, require further elucidation.
Purpose of the Study:
- To investigate the association between endothelial dysfunction and inflammation in patients with slow coronary flow (SCF).
Main Methods:
- Compared 26 SCF patients with 25 controls using TIMI frame count for coronary flow.
- Assessed endothelial function via plasma ADMA, flow-mediated dilatation (FMD), and nitroglycerin-mediated dilatation (NMD).
- Measured inflammation using high-sensitivity C-reactive protein (hs-CRP).
Main Results:
- SCF patients exhibited significantly higher TIMI frame counts, lower FMD, and higher ADMA levels compared to controls.
- No significant differences in NMD or hs-CRP were observed between groups.
- ADMA and FMD were significant predictors of SCF in multivariate analysis, while hs-CRP was not.
Conclusions:
- Endothelial dysfunction, characterized by elevated ADMA and impaired FMD, is implicated in the pathogenesis of slow coronary flow.
- Inflammation, as assessed by hs-CRP, does not appear to play a significant role in the development of SCF.
Objectives:
We evaluated the effects of endothelial dysfunction and inflammation on slow coronary flow (SCF).
Study Design:
The study included 26 patients (group 1; 13 females, 13 males; mean age 58.8 years) who had normal coronary arteries but SCF in three coronary vessels and 25 subjects (group 2, 14 females, 11 males; mean age 62.7 years) with normal coronary arteries and normal flow. Coronary flow was quantified according to the TIMI (Thrombolysis In Myocardial Infarction) frame count method for the left anterior descending (LAD), circumflex (Cx), and right coronary (RCA) arteries. Endothelial function was assessed by plasma asymmetric dimethylarginine (ADMA) levels, brachial artery endothelium-dependent flow-mediated dilatation (FMD), and nitroglycerin-mediated dilatation (NMD). Inflammation was assessed by high-sensitivity C-reactive protein (hs-CRP) levels.
Results:
TIMI frame count was significantly higher in group 1 compared to group 2 for each artery (p<0.001). In group 1, the mean FMD was significantly lower (6.6±1.6% vs. 11.2±1.6%, p<0.001) and the mean ADMA level was significantly higher (0.8±0.2 µmol/l vs. 0.5±0.1 µmol/l, p=0.002), whereas NMD and hs-CRP levels did not differ significantly between the two groups (p>0.05). There was a significant correlation between plasma ADMA level and TIMI frame count (RCA: r=0.50, p=0.001; cLAD: r=0.46, p=0.004; Cx: r=0.32, p=0.04) and a significant negative correlation between FMD and TIMI frame count (cLAD: r=-0.68, p=0.0003; Cx: r=-0.54, p=0.0004; RCA: r=-0.46, p=0.004), but hs-CRP level was not correlated with TIMI frame count. In multivariate analysis, only ADMA (p=0.009) and FMD (p=0.02) were significant parameters to predict SCF.
Conclusion:
Our results suggest that endothelial dysfunction as determined by increased ADMA level and impaired FMD, rather than inflammation, plays a role in the etiopathogenesis of SCF.
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