BACKGROUND: The mechanisms underlying acute cerebrovascular syndrome in patients with carotid artery stenosis remain unclear. OBJECTIVE: To assess the relationships among infarct localization, hemodynamics, and plaque components. METHODS: This prospective study included 38 patients with acute cerebrovascular syndrome resulting from ipsilateral carotid artery stenosis. Cerebral infarct localization was categorized into 3 patterns (cortical, border zone, and mixed pattern). Carotid plaque components were evaluated with T1-weighted magnetic resonance imaging and time-of-flight imaging. Cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) were also quantified. RESULTS: Infarcts were identified in 38 patients with the use of diffusion-weighted magnetic resonance imaging. On the basis of the assessment of hemodynamics, the cortical pattern was seen in 18 of 21 patients with type 1 ischemia (normal CBF, normal CVR), whereas the mixed pattern was seen in 2 patients with type 2 ischemia (normal CBF, impaired CVR) and 12 of 15 patients with type 3 ischemia (impaired CBF, impaired CVR). The plaque components were categorized into fibrous (4 patients), lipid-rich (14 patients), and intraplaque hemorrhage (IPH; 20 patients). Of the patients with fibrous plaque, 2 had border-zone and 2 had mixed-pattern infarcts. Of the patients with lipid-rich plaque, 7 had cortical and 6 had mixed-pattern infarcts. Of patients with intraplaque hemorrhage, 11 had cortical and 9 had mixed-pattern infarcts. CONCLUSION: Cortical infarction occurs as a result of vulnerable plaque. Reduced cerebral perfusion induces border-zone infarction. Both factors are implicated in mixed-pattern infarction. Developments in noninvasive diagnostic modalities allow us to explore the mechanisms behind acute cerebrovascular syndrome in carotid artery stenosis and to determine the ideal therapies.
BACKGROUND: The mechanisms underlying acute cerebrovascular syndrome in patients with carotid artery stenosis remain unclear. OBJECTIVE: To assess the relationships among infarct localization, hemodynamics, and plaque components. METHODS: This prospective study included 38 patients with acute cerebrovascular syndrome resulting from ipsilateral carotid artery stenosis. Cerebral infarct localization was categorized into 3 patterns (cortical, border zone, and mixed pattern). Carotid plaque components were evaluated with T1-weighted magnetic resonance imaging and time-of-flight imaging. Cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) were also quantified. RESULTS:Infarcts were identified in 38 patients with the use of diffusion-weighted magnetic resonance imaging. On the basis of the assessment of hemodynamics, the cortical pattern was seen in 18 of 21 patients with type 1 ischemia (normal CBF, normal CVR), whereas the mixed pattern was seen in 2 patients with type 2 ischemia (normal CBF, impaired CVR) and 12 of 15 patients with type 3 ischemia (impaired CBF, impaired CVR). The plaque components were categorized into fibrous (4 patients), lipid-rich (14 patients), and intraplaque hemorrhage (IPH; 20 patients). Of the patients with fibrous plaque, 2 had border-zone and 2 had mixed-pattern infarcts. Of the patients with lipid-rich plaque, 7 had cortical and 6 had mixed-pattern infarcts. Of patients with intraplaque hemorrhage, 11 had cortical and 9 had mixed-pattern infarcts. CONCLUSION:Cortical infarction occurs as a result of vulnerable plaque. Reduced cerebral perfusion induces border-zone infarction. Both factors are implicated in mixed-pattern infarction. Developments in noninvasive diagnostic modalities allow us to explore the mechanisms behind acute cerebrovascular syndrome in carotid artery stenosis and to determine the ideal therapies.