(Stroke. 1996;27:44-48.)
© 1996 American Heart Association, Inc.
Articles |
From the Departments of Pathology (R.D.P., X.-Y.L.) and Neurology (N.B., B.M.C.), Oregon Health Sciences University, and the Veteran's Affairs Medical Center (N.B., B.M.C.), Portland, Ore.
Correspondence to Oregon Health Sciences University, Department of Pathology, Mail Code L113, 3181 SW Sam Jackson Park Rd, Portland, OR 97201-3098. E-mail pressr@ohsu.edu.
Background and Purpose A common missense mutation in coagulation factor V (Arg 506 Gln) creates phenotypic resistance to the anticoagulant effects of activated protein C and predisposes carriers to venous thrombosis. To assess a correlation between this common hypercoagulable state and ischemic cerebrovascular disease, we have compared the prevalence of this mutation in a group of stroke patients with that in several control patient groups.
Methods The presence of the factor V Arg 506 Gln mutation was determined by a direct polymerase chain reactionbased assay on peripheral blood leukocytes from 161 elderly patients with acute ischemic stroke, 116 elderly patients with stroke risk factors but without acute stroke, 54 healthy elderly control subjects, and 287 younger control individuals (197 blood donors and 90 neonates).
Results The prevalence of the heterozygous Arg 506 Gln
factor V mutation was not significantly different in the elderly stroke
patients (2.5%) compared with either of the age-matched control
groups (2% to 4%). The prevalence of this mutation was significantly
higher in each of two younger control groups (
8%) than in the
elderly stroke patients (2.5%).
Conclusions The common factor V Arg 506 Gln mutation predisposing to venous thrombosis is not a significant genetic risk factor for ischemic stroke in the elderly.
Key Words: blood coagulation cerebrovascular disorders mutation risk factors thrombosis
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