BACKGROUND AND PURPOSE: It has been suggested that daily intake of aspirin
is associated with a reduction of cognitive decline, both in normal and in
demented subjects, but the mechanism is unclear. We have therefore studied
the relationship between thromboxane (TX) A(2) biosynthesis, as reflected
by the urinary excretion of 11-dehydro-TXB(2), and the presence of
dementia in patients after acute stroke. METHODS: Patients from the
Rotterdam Stroke Databank were screened for dementia between 3 and 9
months after stroke. Patients had a full neurological examination,
neuropsychological screening, and, if indicated, extensive
neuropsychological examination. Criteria used for the diagnosis of
dementia were from the Diagnostic and Statistical Manual of Mental
Disorders, Third Edition (Revised). Urine samples were taken at the time
of screening. Urinary 11-dehydro-TXB(2) was measured by means of a
previously validated radioimmunoassay. RESULTS: Dementia was diagnosed in
71 patients, and urine samples were available for 62. Median value (range)
of 11-dehydro-TXB(2) was 399 (89 to 2105) pmol/mmol creatinine for
demented patients versus 273 (80 to 1957) for 69 controls with stroke but
without dementia (P=0.013). No difference was found between 44 patients
with vascular dementia, 404 (89 to 2105) pmol/mmol creatinine, and 18
patients with Alzheimer's disease plus cerebrovascular disease, 399 (96 to
1467) pmol/mmol creatinine (P=0.68). In a stepwise logistic regression
analysis, in which possible confounders such as use of antiplatelet
medication, cardiovascular risk factors, and type of stroke were taken
into account, increased urinary excretion of 11-dehydro-TXB(2) remained
independently related to the presence of dementia (OR 1.12, 95% CI 1.03 to
1.22 per 100 pmol/mmol creatinine). The difference in metabolite excretion
rates between demented and nondemented patients was most prominent within
the subgroup of ischemic stroke patients who received aspirin (P<0.01).
CONCLUSIONS: Increased thromboxane biosynthesis in the chronic phase after
stroke is associated with the presence of but not the type of poststroke
dementia. It is particularly apparent in patients on aspirin, thereby
suggesting the involvement of extraplatelet sources of TXA(2) production
in this setting