D K Jung1, G Devuyst, P Maeder, J Bogousslavsky. 1. Department of Neurology, Centre Hospitalier Universitaire Vaudois, CH-1011, Lausanne, Switzerland. Denise.Allasia@chuv.hospvd.ch
Abstract
OBJECTIVES: To evaluate the characteristics of cardioembolic small (maximum lesion diameter<1.5 cm) subcortical infarcts (SSI) in patients with atrial fibrillation (AF). METHODS: Twenty seven patients with chronic AF and an isolated SSI established by CT/MRI in the anterior circulation (SSI-AF group) were evaluated and their characteristics compared with those of 45 age matched (+/-1 year) patients with SSI, but no arterial or cardiac embolic source (SSI-control group). Using the criterion of the presence or absence of established risk factors (hypertension or diabetes mellitus) for small artery disease (SAD), the SSI-AF group we also subdivided into two groups, SSI-AF-SAD+ (n=22) and SSI-AF-SAD- (n=5) and their characteristics compared. RESULTS: Although the lack of any significant difference in the distribution of hypertension and diabetes mellitus between the SSI-AF and SSI-control groups emphasises SAD as a common cause of infarct in SSI-AF, the presence of AF-together with the higher frequency of neuropsychological disturbances in the SSI-AF group versus the SSI-control group (15% v 2%; p=0.066)-favours cardioembolism as a potential cause of infarct in several patients. The characteristic factors seen more often in the SSI-AF-SAD- group compared with the SSI-AF-SAD+ group were secondary haemorrhagic transformation, faciobrachial pure motor weakness, subinsular involvement, and better recovery of neurological deficits. CONCLUSIONS: The study suggests that either SAD or cardioembolism can be the cause of SSI in patients with AF. Atrial fibrillation is not always coincidental in patients with SSI and a clinical lacunar stroke. Certain clinical and radiological findings may be useful in differentiating cardioembolism from SAD in patients with SSI.
OBJECTIVES: To evaluate the characteristics of cardioembolic small (maximum lesion diameter<1.5 cm) subcortical infarcts (SSI) in patients with atrial fibrillation (AF). METHODS: Twenty seven patients with chronic AF and an isolated SSI established by CT/MRI in the anterior circulation (SSI-AF group) were evaluated and their characteristics compared with those of 45 age matched (+/-1 year) patients with SSI, but no arterial or cardiac embolic source (SSI-control group). Using the criterion of the presence or absence of established risk factors (hypertension or diabetes mellitus) for small artery disease (SAD), the SSI-AF group we also subdivided into two groups, SSI-AF-SAD+ (n=22) and SSI-AF-SAD- (n=5) and their characteristics compared. RESULTS: Although the lack of any significant difference in the distribution of hypertension and diabetes mellitus between the SSI-AF and SSI-control groups emphasises SAD as a common cause of infarct in SSI-AF, the presence of AF-together with the higher frequency of neuropsychological disturbances in the SSI-AF group versus the SSI-control group (15% v 2%; p=0.066)-favours cardioembolism as a potential cause of infarct in several patients. The characteristic factors seen more often in the SSI-AF-SAD- group compared with the SSI-AF-SAD+ group were secondary haemorrhagic transformation, faciobrachial pure motor weakness, subinsular involvement, and better recovery of neurological deficits. CONCLUSIONS: The study suggests that either SAD or cardioembolism can be the cause of SSI in patients with AF. Atrial fibrillation is not always coincidental in patients with SSI and a clinical lacunar stroke. Certain clinical and radiological findings may be useful in differentiating cardioembolism from SAD in patients with SSI.
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