title: Reduced antiplatelet effect of aspirin during 24 hours in patients with coronary artery disease and type 2 diabetes.
abstract: Reduced antiplatelet effect of aspirin has been reported in patients with type 2 diabetes, and recent studies suggest that once-daily aspirin provides insufficient platelet inhibition. We investigated if the effect of aspirin declined during the 24-hour dosing interval in patients with coronary artery disease and type 2 diabetes, and whether this correlated with increased platelet turnover. Furthermore, the intra-individual variation in platelet aggregation was determined during a 28-day period. We included 47 patients with coronary artery disease and type 2 diabetes treated with aspirin 75 mg daily. Blood samples were obtained 1 and 24 hours after aspirin intake, and this was repeated three times with a 2-week interval between each visit. Platelet aggregation was evaluated by impedance aggregometry (Multiplate® Analyzer) using arachidonic acid (1.0 mM) and collagen (3.2 µg/ml) as agonists. Markers of platelet turnover were measured by flow cytometry. Compliance was confirmed by serum thromboxane B2. Platelet aggregation levels measured 1 and 24 hours after aspirin intake were compared using the mean of 1- and 24-hour measurements at the three study visits. The difference in platelet aggregation was 70 ± 97 AU × min (p < 0.0001) when using arachidonic acid as agonist and 33 ± 76 AU × min (p = 0.01) when using collagen. Markers of platelet turnover correlated positively, though not significantly, with residual platelet aggregation 24 hours after aspirin intake (p values 0.06 and 0.07). Median intra-individual variation of platelet aggregation was 9-16%. Patients with coronary artery disease and type 2 diabetes had increased platelet aggregation at the end of the 24-hour aspirin dosing interval. Platelet turnover did not correlate significantly with residual platelet aggregation, although a trend was observed. The intra-individual variation of platelet aggregation after aspirin intake was low.
authors.affiliation: Department of Cardiology and.
authors.forename: Kristian H
authors.initials: KH
authors.lastname: Christensen
authors.forename: Erik L
authors.initials: EL
authors.lastname: Grove
authors.forename: Morten
authors.initials: M
authors.lastname: Würtz
authors.forename: Steen D
authors.initials: SD
authors.lastname: Kristensen
authors.forename: Anne-Mette
authors.initials: AM
authors.lastname: Hvas
mesh_terms: D000368:Aged; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000188:drug therapy* / Q000378:metabolism* / Q000628:therapy; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis / Q000188:drug therapy* / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D013929:Thromboxane B2 / Q000097:blood; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D010975:Platelet Aggregation Inhibitors; D013929:Thromboxane B2; D001241:Aspirin
keywords: Aspirin; coronary artery disease; diabetes mellitus; platelet aggregation; platelet function tests; platelet turnover