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Cerebrovasc Dis. 2002;13(1):16-20.

Carotid artery stenosis in ischemic stroke patients with nonvalvular atrial fibrillation.

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Department of Neurology, Chang Gung Memorial Hospital, Taipei, Taiwan.



To study the prevalence, severity and clinical relevance of carotid atherosclerosis in ischemic stroke patients with nonvalvular atrial fibrillation (NVAF).


We reviewed carotid duplex sonography, computed tomography (CT) and clinical features in 103 consecutive ischemic stroke patients with NVAF. Both sonography and CT were performed within 3-7 days after stroke. There were 64 men and 39 women with a mean age at stroke onset of 69 years.


High-grade (> or =50%) stenosis of the extracranial carotid artery was detected in 25 patients (24.3%), including 11 patients (10.6%) with internal carotid artery (ICA) occlusion. In 15 (66.7%) of the patients who had high-grade carotid stenosis, the lesion was ipsilateral to the infarct, including 8 ICA occlusions. Patients with high-grade stenosis smoked more cigarettes (p < 0.05) and had more peripheral vascular diseases (p < 0.05). Besides NVAF, all patients had more than one vascular risk factor. The clinical presentations (transient ischemic attacks, minor or major strokes) showed no significant difference between the groups of <50% and > or =50% stenosis. Clinical outcome was worse (dead and totally dependent in daily activities) in the group of high-grade stenosis (p < 0.05). Patients with high-grade carotid stenosis showed more cortical infarcts on cerebral CT (p < 0.01). Six out of 7 patients with a hemorrhagic transformation on the initial cerebral CT were in the low-grade carotid stenosis group, though this was statistically insignificant.


Ischemic stroke with NVAF is not always cardiogenic. High-grade stenosis of the extracranial carotid artery is found in one fourth of ischemic stroke patients with NVAF and is related to more cortical infarction and worse clinical outcome. We speculate that ischemic stroke patients with NVAF who have high-grade carotid stenosis are less likely to develop hemorrhagic infarct. The pathogenesis of cerebral infarction and the therapeutic strategy in this clinical condition are complicated by the coexistence of carotid arterial lesions and cardiac disease.

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