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- Title
Comparison of antiplatelet activity of microencapsulated aspirin 162.5 mg (Caspac XL), with enteric coated aspirin 75 mg and 150 mg in patients with atherosclerosis.
- Authors
Brown, Nigel; May, Jane A.; Wilcox, Robert G.; Allan, Linda M.; Wilson, Adrian M.; Kiff, Peter S.; Heptinstall, Stan
- Abstract
Aims A new formulation, low dose microencapsulated aspirin, permits slow absorption of aspirin and presystemic acetylation of platelet cyclo-oxygenase within the portal circulation, potentially avoiding deleterious effects on gastric and systemic prostaglandin synthesis. The objective of this study was to determine whether the administration of microencapsulated aspirin was as effective as enteric coated (EC) aspirin as an inhibitor of platelet function in patients with atherosclerosis. Methods One hundred and four patients were enrolled and randomised after a run in period of at least 14 days on aspirin EC 75 mg (day 0), to receive either microencapsulated aspirin 162.5 mg (n=34), aspirin EC 150 mg (n=36) or continue on aspirin EC 75 mg (n=34) for 28 days. Serum thromboxane B[sub 2] and collagen-induced platelet aggregation and release of 5-hydroxytryptamine (EC[sub 50] values) were measured on days 0 and 28. Aggregation/release EC[sub 50]s were then repeated in the presence of a large dose of aspirin added in vitro to determine the EC[sub 50] at the maximum level of platelet inhibition. Results Median thromboxane B[sub 2] levels were low after 14 days run-in therapy with aspirin EC 75 mg, but significant further reductions were seen on day 28 in patients randomised to microencapsulated aspirin 162.5 mg (P=0.0368) and aspirin EC 150 mg (P=0.0004) compared with those remaining on aspirin EC 75 mg. Median EC[sub 50] s on day 28 showed small but significant increases from baseline (day 0) in aggregation in patients randomised to microencapsulated aspirin 162.5 mg (0.62–0.85, P=0.0482) and in both aggregation and release in patients randomised to aspirin EC 150 mg (0.95–1.20, P=0.0002, 8.4–11.7, P<0.0001, respectively) signifying enhanced antiplatelet activity. No changes were seen in patients continuing on aspirin EC 75 mg. Results following addition of high dose aspirin in vitro suggest that mechanisms other than thromboxane synthesis m...
- Subjects
ASPIRIN; ATHEROSCLEROSIS; PHYSIOLOGY; PATIENTS
- Publication
British Journal of Clinical Pharmacology, 1999, Vol 48, Issue 1
- ISSN
0306-5251
- Publication type
Article
- DOI
10.1046/j.1365-2125.1999.00947.x