Related Experiment Video
Updated: Jun 22, 2026

Middle Cerebral Artery Occlusion Allowing Reperfusion via Common Carotid Artery Repair in Mice
Published on: January 23, 2019
Endothelial function in lacunar infarction: a comparison of lacunar infarction, cerebral atherosclerosis and control
Jin-Seok Kim1, Hak-Seung Lee, Hyun-Young Park
1Department of Neurology, Wonkwang University School of Medicine, Jeonbuk, South Korea.
Insights
Endothelial function, measured by flow-mediated dilatation (FMD), is impaired in patients with lacunar infarction, suggesting pure endothelial dysfunction. Nitrogen-mediated dilatation (NMD) showed no significant difference, indicating specific damage to the endothelium in these patients.
Area of Science:
- Neurology
- Vascular Biology
- Cardiology
Background:
- Conflicting evidence exists regarding endothelial function in lacunar infarction.
- Risk factors may influence vascular smooth muscle, complicating assessments.
- This study isolates endothelial function in lacunar infarction patients.
Purpose of the Study:
- To evaluate endothelium-dependent and -independent vasodilation in lacunar infarction patients.
- To differentiate endothelial dysfunction from other vascular effects.
- To compare endothelial function in lacunar infarction with controls.
Main Methods:
- Enrolled patients with lacunar infarction (clinical and MRI confirmed).
- Used a control group of age/sex-matched hypertensive patients without stroke or vascular disease.
- Assessed endothelial function via brachial artery flow-mediated dilatation (FMD) and nitrogen-mediated dilatation (NMD) using high-resolution ultrasound.
Main Results:
- Flow-mediated dilatation (FMD) was significantly lower in lacunar infarction patients (6.6%) compared to controls (12.2%, p=0.000).
- Nitrogen-mediated dilatation (NMD) showed no significant difference between groups (14.3% vs 13.8%, p=0.37).
- FMD was similarly low in lacunar infarction patients with and without intracranial stenosis.
Conclusions:
- Lacunar infarction is associated with impaired endothelial function, indicated by reduced FMD.
- The similar NMD suggests specific endothelial dysfunction, not generalized vascular smooth muscle issues.
- Endothelial dysfunction in lacunar infarction is comparable in severity to that seen in intracranial arterial stenosis.
Background:
There are conflicting evidences on endothelial function in lacunar infarction. This may be attributed to the effects of risk factors on the vascular smooth muscle. To test endothelial function only in patients with lacunar infarction, we evaluated the endothelium-dependent and -independent vasodilatation of the brachial artery.
Methods:
We enrolled consecutive patients with lacunar infarction defined by clinical characteristics and MRI findings. The control group included age- and sex-matched patients with hypertension who do not have any history of clinical stroke, coronary artery disease or peripheral vascular disease. Endothelial function was evaluated using flow-mediated dilatation (FMD) and nitrogen-mediated dilatation (NMD) of the brachial artery. FMD and NMD were examined by an experienced vascular sonographer using a high-resolution ultrasound. Intracranial stenosis was defined as flow gap or >50% reduction in vessel diameter on MRA.
Results:
FMD was 6.6 +/- 4.5% in the lacunar infarction group and 12.2 +/- 4.6% in the control group (p = 0.000). NMD was 14.3 +/- 4.9% in the lacunar infarction group and 13.8 +/- 4.9% in the control group (p = 0.37). FMD in patients with lacunar infarction and intracranial arterial stenosis was 6.4 +/- 3.9%, and FMD in patients with lacunar infarction was only 6.9 +/- 5.5%. In the control group, it was 12.2 +/- 4.6%.
Conclusion:
FMD was low in patients with lacunar infarction. NMD was similar between the lacunar infarction group and the control group. These results are suggestive of pure endothelial dysfunction in lacunar infarction. Endothelial dysfunction was as severe in lacunar infarction as in intracranial arterial stenosis.
Related Concept Videos
Ischemic Stroke l: Introduction
Atherosclerosis I: Introduction
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests
Ischemic Stroke ll: Pathophysiology