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(Stroke. 2002;33:57.)
© 2002 American Heart Association, Inc.

Original Contributions

Aspirin and Urinary 11-Dehydrothromboxane B₂ in African American Stroke Patients

Askiel Bruno, MD; Joseph P. McConnell, PhD; Harry H. Mansbach, III, MD; Stanley N. Cohen; Gretchen E. Tietjen, MD Nils U. Bang, MD

From Indiana University School of Medicine (A.B., N.U.B.), Indianapolis, Ind; the Mayo Clinic (J.P.M.), Rochester, Minn; GlaxoSmithKline (H.H.M.), Research Triangle Park, NC; Veterans Affairs Greater Los Angeles Healthcare System (S.N.C.), Los Angeles, Calif; and the Medical College of Ohio (G.E.T.), Toledo.

Correspondence to Askiel Bruno, MD, Neurology Department, 541 Clinical Dr, R.365, Indianapolis, IN 46202-5111. E-mail abruno{at}iupui.edu

Background and Purpose— The aim of the study was to evaluate the relationship between daily aspirin use and urinary excretion of a stable thromboxane metabolite, 11-dehydrothromboxane B₂ (11-DTB2), in African American stroke patients.

Methods— Subjects were a subgroup of those screened for the African American Antiplatelet Stroke Prevention Study. Subjects were within 4 months of noncardioembolic ischemic stroke and were not being treated with anticoagulants. Antithrombotic therapy at the time of urine collection varied according to the practice patterns of various attending physicians who treated the patients during their acute strokes. 11-DTB2 was measured by enzyme immunoassay in random urine samples 1 to 4 months after the stroke.

Results— Eighty-seven of 92 patients enrolled were able to give a urine sample at the time of enrollment. There were 51 men and 36 women aged 36 to 87 (mean 62) years. On the basis of antithrombotic treatment before the sample collection, we divided patients into 4 groups: (1) 16 patients treated with no aspirin (no antithrombotic drugs [n=4] or ticlopidine [n=12]), (2) 21 patients treated with 81 to 325 mg aspirin per day (81 mg/d [n=2], 325 mg/d [n=19]), (3) 20 patients treated with 650 mg aspirin per day, and (4) 30 patients treated with 975 to 1300 mg aspirin per day (975 mg/d [n=2] and 1300 mg/d [n=28]). In patients taking daily aspirin at any dose, the median urinary 11-DTB2 was 783 pg/mg creatinine compared with 1386 pg/mg creatinine in patients not taking daily aspirin (P=0.01 by Wilcoxon rank sum test). In multivariate regression analysis, aspirin use remained significantly associated with lower urinary 11-DTB2 (P=0.008). There was no dose-response effect between the 3 aspirin dose groups and urinary 11-DTB2 (P=0.70).

Conclusions— In African American stroke patients, aspirin use is associated with significantly lower urinary 11-DTB2 independent of other vascular factors, and there does not appear to be a dose-response effect for aspirin doses of 325 to 1300 mg daily. The clinical significance of these finding remains to be determined.

Key Words: aspirin • cerebral infarction • platelets • thrombosis

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