Aspirin dose and thromboxane metabolism in African American stroke patients
Purpose:To evaluate thromboxane metabolism in African American stroke patients on different doses of aspirin. Methods:Consecutive African American patients within 3 month of non-cardioembolic stroke and not being treated with anticoagulation were recruited. Antithrombotic therapy at the time of sample collection was not prespecified and varied according to the practice patterns of the different attending physicians who treated the patients during their acute stroke. The thromboxane metabolite 11-dehydrothroboxane B2 (11-DTB2) was measured by enzyme immunoassay in random urine samples collected at the time of enrollment. Results:99 patients were enrolled but 15 could not give a urine sample at the time of enrollment. Data on the remaining 84 patients were evaluable. There were 49 men and 35 women aged 36–87 (mean 62) years. Based on antithrombotic treatment during sample collections, we divided patients into four groups: no aspirin N=16 (no antithrombotic drugs N=4 or ticlopidine N=12), aspirin 81–325 mg/d N=19 (81 mg/day N=1, 325 mg/day N=18), aspirin 650 mg/d N=19, aspirin 975–1300 mg/d N=30 (975 mg/d N=2 and 1300 mg/d N=28). After log transformation of the 11-DTB2 values the geometric means in the no aspirin, 81–325 mg/d, 650 mg/d, and 975–1300 mg/d groups were 1355, 912, 758, and 731 pg/mg creatinine, respectively. Based on one way ANOVA, the mean 11-DTB2 concentration was significantly different between the 4 groups (p=0.03). There was a significant negative relationship between aspirin dose and 11-DTB2 concentration (Pearson Correlation, r = -0.26, P=0.02). Conclusion:In African American stroke patients thromboxane production appears to be progressively inhibited by aspirin doses up to 650 mg/d. The clinical significance of this effect by aspirin doses ≤650 mg/d remains to be determined.