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J Neurol Neurosurg Psychiatry 2001;70:344-349 doi:10.1136/jnnp.70.3.344
  • Paper

Atrial fibrillation with small subcortical infarcts

  1. D K Junga,
  2. G Devuysta,
  3. P Maederb,
  4. J Bogousslavskya
  1. aDepartment of Neurology, Centre Hospitalier Universitaire Vaudois, CH-1011, Lausanne, Switzerland, bDepartment of Radiology
  1. Dr D K JungDenise.Allasia{at}chuv.hospvd.ch
  • Received 25 January 2000
  • Revised 2 October 2000
  • Accepted 11 October 2000

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.

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