Sonographic Evaluation of Endothelial Function in Brachial Arteries of Adult Stroke Patients.

OBJECTIVES: Brachial artery flow-mediated dilatation on sonography is used to evaluate endothelial dysfunction, which is a key event in the development of atherosclerosis and predates structural atherosclerotic lesions by many years. Atherosclerosis has been implicated in the pathophysiologic mechanisms of ischemic stroke. The aim of this study was to determine the association between brachial flow-mediated dilatation, the presence of cardiovascular risk factors, and acute stroke. METHODS: We evaluated right brachial arteries of 150 participants (50 stroke patients, 50 patients with cardiovascular risk factors, and 50 healthy control individuals) with B-mode sonography before and 5 minutes after sphygmomanometer cuff application to their forearms. Analysis of variance for multiple comparisons was used between each group. RESULTS: Mean ages of the stroke, risk factor, and control groups ± SD were 57.5 ± 14.8, 52.4 ± 16.0, and 56.1 ± 14.9 years, respectively (P = .235). Flow-mediated dilatation rates were 4.37% ± 1.50%, 5.62% ± 1.23%, and 10.33% ± 1.96% in the stroke, risk factor, and control groups (P ≤ .001). Dilatation was 3.79% ± 0.92% in ischemic stroke compared with 6.02% ± 1.62% in intracerebral hemorrhage (P < .001), but there was no significant difference in dilatation between ischemic stroke subtypes according to the Trial of ORG 10172 in Acute Stroke Treatment classification (P = .301). CONCLUSIONS: Brachial flow-mediated dilatation was significantly lower in patients with acute stroke compared with controls matched for vascular risk factors and healthy controls. Decreased vascular endothelial function in stroke patients was particularly related to cerebral infarction compared with intracerebral hemorrhage. Brachial flow-mediated dilatation did not differentiate ischemic stroke subtypes by the Trial of ORG 10172 in Acute Stroke Treatment classification. Flow-mediated dilatation was therefore found to be a marker of cardiovascular risk and a probable reactant in the acute phase of stroke.