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(Stroke. 2004;35:727.)
© 2004 American Heart Association, Inc.

Original Contributions

Serial Urinary 11-Dehydrothromboxane B2, Aspirin Dose, and Vascular Events in Blacks After Recent Cerebral Infarction

Askiel Bruno, MD; Joseph P. McConnell, PhD; Stanley N. Cohen, MD; Gretchen E. Tietjen, MD; Roi Ann Wallis, MD; Philip B. Gorelick, MD, MPH Nils U. Bang, MD

From Indiana University School of Medicine, Indianapolis (A.B., N.U.B.); Mayo Clinic, Rochester, Minn (J.P.M.); Cedars Sinai Medical Center, Los Angeles, Calif (S.N.C.); Medical College of Ohio, Toledo, Ohio (G.E.T.); West Los Angeles Veterans Affairs Medical Center, Los Angeles, Calif (R.A.W.); and Rush–Presbyterian–St Luke’s Medical Center, Chicago, Ill (P.B.G.).

Correspondence to Askiel Bruno, MD, Neurology Department, 541 Clinical Dr, Room 290C, Indianapolis, IN 46202-5111. E-mail abruno{at}iupui.edu

Background and Purpose— Incomplete platelet inhibition by aspirin (aspirin resistance) may be a reason for stroke recurrence in some patients. 11-Dehydrothromboxane B2 (11-DTB2) is a stable thromboxane A2 metabolite that reflects in vivo platelet activation. This pilot study was intended to evaluate the reproducibility of urinary 11-DTB2 over time and to look for evidence of aspirin resistance.

Methods— All subjects were screened for the African American Antiplatelet Stroke Prevention Study (AAASPS) 7 to 90 days after noncardioembolic cerebral infarction. Of 83 subjects with at least 1 urine sample, 52 were enrolled in AAASPS (randomized to blinded treatment with aspirin 650 mg/d or ticlopidine 500 mg/d), and 31 were enrolled in an open-label antiplatelet therapy cohort. Subjects were followed up for 2 years, with 11-DTB2 measurements scheduled at baseline and 6, 12, and 24 months. Vascular events were cerebral infarction, myocardial infarction, or vascular death.

Results— Despite considerable individual up or down fluctuations, the median 11-DTB2 change did not significantly differ from zero in any of the subgroups. However, in 6 subjects with a 4-fold decrease in aspirin dose from 1300 to 325 or 81 mg/d, the 11-DTB2 level increased from 611 to 1881 pg/mg creatinine (P=0.06). Vascular events occurred in 7 of 61 aspirin-treated subjects, and 11-DTB2 levels did not correlate with the events.

Conclusions— Fluctuations in urinary 11-DTB2 after cerebral infarction in blacks do not correlate with changes in aspirin doses, except perhaps when the dose changes by a factor of 4 or more. A larger study is needed to look further for aspirin resistance.

Key Words: aspirin • cerebral infarction • platelets

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