Abstract
BackgroundAspirin is a cornerstone in management of coronary artery disease (CAD). However, considerable variability in the antiplatelet effect of aspirin has been reported.AimTo investigate independent determinants of reduced antiplatelet effect of aspirin in stable CAD patients.MethodsWe performed a cross-sectional study including 900 stable, high-risk CAD patients. Among these, 795 (88%) had prior myocardial infarction, 250 (28%) had type 2 diabetes, and 170 (19%) had both. All patients received 75 mg aspirin daily as mono antiplatelet therapy. The antiplatelet effect of aspirin was assessed by measurement of platelet aggregation employing 1) multiple electrode aggregometry (MEA, Multiplate Analyzer) in whole blood anticoagulated with citrate or hirudin using arachidonic acid (AA) or collagen as agonists, and 2) VerifyNow Aspirin Assay. Compliance was assessed by measurement of serum thromboxane B2.ResultsPlatelet count, prior myocardial infarction, type 2 diabetes and body mass index were independent determinants of increased AA-induced MEA platelet aggregation in citrate and hirudin anticoagulated blood (p-values ≤ 0.045). Similar results were found with VerifyNow. Prior coronary artery bypass grafting, age, smoking (MEA, AA/citrate) and female gender (MEA, AA/hirudin) were also independent determinants of increased platelet aggregation (p-values ≤ 0.038). Compliance was confirmed by low serum thromboxane B2 levels in all patients (median [25%;75%]: 0.97 [0.52;1.97], range 0.02-26.44 ng/ml).ConclusionPlatelet count, prior myocardial infarction, type 2 diabetes and body mass index were independent determinants of increased platelet aggregation, indicating that these characteristics may be key factors in reduced antiplatelet effect of aspirin in stable CAD patients.
Highlights
Low-dose aspirin is recommended for patients with stable coronary artery disease (CAD) [1]
The antiplatelet effect of aspirin was assessed by measurement of platelet aggregation employing 1) multiple electrode aggregometry (MEA, Multiplate Analyzer) in whole blood anticoagulated with citrate or hirudin using arachidonic acid (AA) or collagen as agonists, and 2) VerifyNow Aspirin Assay
We studied a population of stable CAD patients with a relatively high-risk profile, since 795 (88%) of the patients had a history of myocardial infarction (MI), 250 (28%) had type 2 diabetes and 170 (19%) had both
Summary
Low-dose aspirin is recommended for patients with stable coronary artery disease (CAD) [1]. Despite extensive research on variability in the antiplatelet effect of aspirin, several issues contribute to the difficulty and complexity of data interpretation. These issues include inconsistent definitions of “aspirin resistance”, differences in platelet function tests including agonists and anticoagulants used as well as cut-off levels applied to define the prevalence of "low-responders", and small or heterogeneous study populations [2,5]. Aspirin is a cornerstone in management of coronary artery disease (CAD). Considerable variability in the antiplatelet effect of aspirin has been reported
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