뇌백질변성에서 혈관내피세포 기능장애
Vascular Endothelial Dysfunction in Cerebral Leukoaraiosis
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초록
Background: Chronic subclinical ischemia has been considered as one of major causes of leukoaraiosis, although its trigger is unknown. The vascular endothelium plays a major role in maintaining cerebral perfusion through autoregulation. In this study we evaluated the endothelial bioavailability of nitric oxide (NO) in patients with leukoaraiosis. Methods: We enrolled consecutive patients with lacunar syndrome or transient ischemic attack; the control group comprised age- and sex-matched patients with hypertension but with no neurological abnormality. All participants underwent flow-mediated dilatation of the brachial artery (FMD) to evaluate endothelial function. Leukoaraiosis was defined as ill-defined patches with high signal intensities on FLAIR and low signal intensities on T1-weighted images. Patients were defined as having ischemic leukoaraiosis if they presented with leukoaraiosis and lacunar infarction. Leukoaraiosis only was defined when patient had leukoaraiosis without lacunar infarction leukoaraiosis without lacunar infarction. Results: In total, 75 patients (37 with leukoaraiosis and 38 controls) were enrolled in this study. The demographic and clinical characteristics were similar in the two groups. FMD was lower in patients with leukoaraiosis than in controls (p<0.05), and lower in patients with only leukoaraiosis and in those who also had ischemic leukoaraiosis than in the controls (p<0.05). However, FMD did not differ significantly between patients with leukoaraiosis only and those who also had ischemic leukoaraiosis (p>0.05). Conclusions: The bioavailability of NO in the vascular endothelium is decreased in patients with leukoaraiosis only and in those who also have ischemic leukoaraiosis compared to controls. These results are suggestive of a causative role of endothelial dysfunction in the pathomechanism of leukoaraiosis.
Abstract
Background: Chronic subclinical ischemia has been considered as one of major causes of leukoaraiosis, although its trigger is unknown. The vascular endothelium plays a major role in maintaining cerebral perfusion through autoregulation. In this study we evaluated the endothelial bioavailability of nitric oxide (NO) in patients with leukoaraiosis. Methods: We enrolled consecutive patients with lacunar syndrome or transient ischemic attack; the control group comprised age- and sex-matched patients with hypertension but with no neurological abnormality. All participants underwent flow-mediated dilatation of the brachial artery (FMD) to evaluate endothelial function. Leukoaraiosis was defined as ill-defined patches with high signal intensities on FLAIR and low signal intensities on T1-weighted images. Patients were defined as having ischemic leukoaraiosis if they presented with leukoaraiosis and lacunar infarction. Leukoaraiosis only was defined when patient had leukoaraiosis without lacunar infarction leukoaraiosis without lacunar infarction. Results: In total, 75 patients (37 with leukoaraiosis and 38 controls) were enrolled in this study. The demographic and clinical characteristics were similar in the two groups. FMD was lower in patients with leukoaraiosis than in controls (p<0.05), and lower in patients with only leukoaraiosis and in those who also had ischemic leukoaraiosis than in the controls (p<0.05). However, FMD did not differ significantly between patients with leukoaraiosis only and those who also had ischemic leukoaraiosis (p>0.05). Conclusions: The bioavailability of NO in the vascular endothelium is decreased in patients with leukoaraiosis only and in those who also have ischemic leukoaraiosis compared to controls. These results are suggestive of a causative role of endothelial dysfunction in the pathomechanism of leukoaraiosis.
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