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Published on: November 3, 2016
Impaired Brachial Flow-Mediated Dilatation May Predict Symptomatic Intracranial Arterial Dissections
Tomonori Iwata1, Takahisa Mori2, Yuhei Tanno2
1Department of Neurology, Tokai University School of Medicine, Isehara City, Kanagawa, Japan.
Insights
Patients with spontaneous intracranial arterial dissections show impaired endothelial function, specifically reduced flow-mediated dilatation, suggesting it may predict dissections. This finding aids in understanding dissection risk factors.
Area of Science:
- Vascular Medicine
- Neurology
- Cardiology
Background:
- Spontaneous intracranial arterial dissections involve disruption of the internal elastic lamina in brain arteries.
- Investigated endothelial function in patients with nontraumatic intracranial arterial dissections.
Observation:
- Compared endothelial function (flow-mediated dilatation) in 22 dissection patients and 22 matched controls.
- Assessed atherosclerosis markers: ankle brachial index and pulse wave velocity.
- No significant differences in ankle brachial index or pulse wave velocity were found between groups.
Findings:
- Patients with intracranial arterial dissections exhibited significantly lower flow-mediated dilatation (3.95%) compared to controls (7.3%).
- Impaired brachial flow-mediated dilatation was observed in symptomatic dissection patients.
- Atherosclerosis markers (ABI, PWV) were normal, indicating endothelial dysfunction is a key factor.
Implications:
- Impaired brachial flow-mediated dilatation may serve as a predictive marker for intracranial arterial dissections.
- Highlights the role of endothelial dysfunction in the pathogenesis of these dissections.
- Suggests potential for early detection and risk stratification in patients with vascular risk factors.
Background And Purpose:
Spontaneous intracranial arterial dissections are characterized by the sudden disruption of the internal elastic lamina in the intracranial arteries. The purpose of our retrospective study was to investigate whether patients with nontraumatic intracranial arterial dissections had normal endothelial function.
Methods:
The study included symptomatic patients with nontraumatic intracranial arterial dissections who underwent an endothelial function test. Controls were selected from headache patients matched for sex and age. Endothelial function was assessed using flow-mediated dilatation. We investigated patients' ankle brachial index and pulse wave velocity to determine the degree of atherosclerosis. Patient characteristics, brachial flow-mediated dilatation, ankle brachial index, and pulse wave velocity were compared between the 2 groups.
Results:
During the study period, there were 22 patients with nontraumatic intracranial arterial dissections matched with 22 controls. Clinical characteristics were compared between the groups. Although there were no significant differences in ankle brachial index or pulse wave velocity between the 2 groups, patients with intracranial arterial dissections had lower flow-mediated dilatation values than controls (median flow-mediated dilatation, 3.95% in dissection patients versus 7.3% in controls, P = .0035). Brachial flow-mediated dilatation was impaired in symptomatic patients with nontraumatic intracranial arterial dissections despite the normal ankle brachial index and pulse wave velocity.
Conclusions:
Impaired brachial flow-mediated dilatation is a probable predictor of intracranial arterial dissections.
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