Aspirin resistance can be classified into three distinct types based on whether oral (100 mg/day) or in vitro aspirin completely (>95%) inhibits platelet aggregation and thromboxane formation.
How can aspirin resistance be classified based on platelet aggregation and thromboxane formation responses?
This study proposes a novel three-type classification system for aspirin resistance based on pharmacokinetic and pharmacodynamic responses, which may help clarify its mechanisms and clinical relevance.
'Aspirin resistance' is a poorly defined term to describe the inability of aspirin to protect individuals from thrombotic complications and there are conflicting reports on incidence rates and clinical relevance of this phenomenon. Using collagen (1 microg/ml)-induced platelet aggregation and thromboxane formation (measured as thromboxane B(2)) in citrated platelet-rich plasma, this study demonstrates that aspirin resistance can be classified into three distinct types. In aspirin responders, both, collagen-induced platelet aggregation and thromboxane formation was completely (>95%) inhibited by oral aspirin treatment (100 mg/day). In type I resistance (pharmacokinetic type), oral treatment with aspirin was ineffective but addition of aspirin (100 microM) in vitro resulted in a complete inhibition of collagen-induced platelet aggregation and thromboxane formation. In type II resistance (pharmacodynamic type), neither oral treatment with aspirin nor addition of aspirin in vitro inhibited collagen-induced platelet aggregation and thromboxane formation. In type III resistance (pseudo-resistance), platelet aggregation was induced by a low concentration of collagen (1 microg/ml) despite of a complete inhibition of thromboxane formation by oral aspirin treatment. This typology of aspirin resistance should help to clarify the mechanisms, the actual rate, and the possible clinical consequences of this phenomenon.
Weber et al. (Tue,) conducted a other in Aspirin resistance. Aspirin was evaluated on Collagen-induced platelet aggregation and thromboxane formation. Aspirin resistance can be classified into three distinct types based on whether oral (100 mg/day) or in vitro aspirin completely (>95%) inhibits platelet aggregation and thromboxane formation.