(Stroke. 1997;28:1932-1939.)
© 1997 American Heart Association, Inc.
Articles |
Subcortical Silent Brain Infarction as a Risk Factor for Clinical Stroke
From the Department of Internal Medicine III, Shimane (Japan) Medical University.
Correspondence to Shotai Kobayashi, Department of Internal Medicine III, Shimane Medical University, Izumo, Shimane, 693, Japan. E-mail skdr3nai{at}shimane-med.ac.jp
Background and Purpose No prospective studies have examined the rate of symptomatic ischemic or hemorrhagic stroke in patients with subcortical silent brain infarction (SSBI) who were otherwise neurologically normal at entry into the study. This report investigates SSBI, detected by MRI, as a clinical stroke risk factor.
Methods MRI scans were performed in 933 neurologically normal adults (30 to 81 years; mean age, 57.5±9.2 years) without history of cerebrovascular diseases who received our health screening of the brain 1 to 7 years before investigation. We obtained information of their clinical stroke onset through sending out a questionnaire for subjects. We detected SSBI (focal T2 hyperintensities larger than 3 mm with correlative T1 hypointensity), FWT2HL (focal white matter T2 hyperintensity lesions similar to SSBI but without correlative T2-hypointensity), and PVH (periventricular hyperintensity) by MRI. Age, sex, family history of stroke, history of hypertension, diabetes mellitus, lipids, hematocrit, blood pressure, fasting blood sugar, smoking, alcohol habits, ischemic changes on electrocardiogram, and sclerotic changes of retinal arteries were included in the analysis.
Results Incidence of SSBI was 10.6% in all subjects. No
cortical infarct was detected in this series. Multiple logistic
regression analysis showed that hypertension (odds ratio
[OR], 4.07; 95% CI, 2.57 to 6.45), diabetes (OR, 2.41; 95% CI, 1.20
to 4.85), alcohol habits 
58 g/day (OR, 2.58; 95% CI, 1.50 to 4.45),
retinal artery sclerosis (OR, 2.14; 95% CI, 1.32 to 2.38), and age
(OR, 1.77; 95% CI, 1.32 to 2.38) were significant and independent risk
factors for SSBI. For FWT2HL, hypertension (OR, 4.49; 95% CI, 2.54 to
7.96) and age (OR, 2.08; 95% CI, 1.45 to 3.00) were also independent
risk factors. Risk factors for PVH were age (OR, 3.46; 95% CI, 2.23 to
5.36), hypertension (OR, 3.06; 95% CI, 1.62 to 5.78), and retinal
artery sclerosis (OR, 2.25; 95% CI, 1.02 to 4.96). We found 14 brain
infarctions, 4 brain hemorrhages, and 1 subarachnoid
hemorrhage during observation. Annual incidence of clinical
stroke was higher in the subjects with SSBI than in those without focal
lesions (10.1% versus 0.77%). ORs for clinical stroke onset were
10.48 for SSBI (95% CI, 3.63 to 30.21) and 4.81 for FWT2HL (95% CI,
1.13 to 20.58). The PVH did not relate to clinical stroke onset.
Conclusions The strong association of SSBI, FWT2HL, and PVH with hypertension suggests a common underlying mechanism (presumably small-vessel vasculopathy). The SSBI showed the most significant association for clinical subcortical stroke. The FWT2HL was also a risk factor for the stroke but was less significant than SSBI. The subjects with SSBI should be considered at high risk for clinical subcortical brain infarction or brain hemorrhage.
Key Words: magnetic resonance imaging • cerebral infarction • cerebral hemorrhage • risk factors
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