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Lack of effect of enteric coating on aspirin-induced inhibition of platelet aggregation in healthy volunteers.

Karha J, Rajagopal V, Kottke-Marchant K, Bhatt DL

Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.

BACKGROUND: Aspirin inhibits platelet aggregation and is widely used in the treatment of cardiovascular disease. Some individuals are less responsive to aspirin's antiplatelet effect, a phenomenon termed aspirin resistance. It is not known whether the antiplatelet effect is fully preserved with the enteric-coated (EC) formulation. METHODS: We performed a prospective randomized trial of 50 healthy volunteers using a crossover design to compare the EC with the standard aspirin formulations. The subjects received a 7-day course of each aspirin formulation (81-mg) (Bayer Corporation, Morristown, NJ) separated by a 3-week washout period. Platelet function was measured before and after each course using optical aggregometry (with arachidonic acid and adenosine diphosphate as agonists) and a point-of-care platelet assay. RESULTS: The assays were reproducible, and the variation in baseline platelet function was small to moderate between the subjects. There was no difference in the extent of platelet inhibition between the EC and standard formulations with any of the 3 assays. With the point-of-care platelet assay, the mean aspirin effect favoring the standard formulation (more aggregation inhibition) compared with the EC formulation was 1.6% +/- 15.8% (P = .60 for difference between the formulations). The corresponding optical aggregometry values were -3.4% +/- 39.5% (P = .97) and -1.4% +/- 16.6% (P = .75) for arachidonic acid and adenosine diphosphate, respectively. CONCLUSIONS: Compared with standard aspirin, EC aspirin appears to exhibit similar inhibition of platelet aggregation in healthy volunteers. Furthermore, point-of-care platelet assessment correlated well with the gold standard of laboratory-based optical platelet aggregometry.

Published 28 April 2006 in Am Heart J, 151(5): 976.e7-11.
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