Results indicated that some PFTs may have some prognostic utility , i.e. a trend for more clinical events to be associated with groups classified as ' aspirin resistant ' .
Study -level effect sizes were generally small and absolute outcome risk was not substantially different between ' aspirin resistant ' and ' aspirin sensitive ' design ations .
Based on assumptions of PFTs being able to accurately identify patients at high risk of clinical events and such patients benefiting from treatment modification , the economic model found that a test-treat strategy was likely to be cost-effective .
However , neither assumption is currently evidence based .
BACKGROUND The use of aspirin is well established for secondary prevention of cardiovascular disease .
However , a proportion of patients suffer repeat cardiovascular events despite being prescribed aspirin treatment .
It is uncertain whether or not this is due to an inherent inability of aspirin to sufficiently modify platelet activity .
This report aims to investigate whether or not insufficient platelet function inhibition by aspirin ( ' aspirin resistance ' ) , as defined using platelet function tests ( PFTs ) , is linked to the occurrence of adverse clinical outcomes , and further , whether or not patients at risk of future adverse clinical events can be identified through PFTs .
OBJECTIVES To review systematic ally the clinical effectiveness and cost-effectiveness evidence regarding the association between PFT design ation of ' aspirin resistance ' and the risk of adverse clinical outcome ( s ) in patients prescribed aspirin therapy .
To undertake exploratory model-based cost-effectiveness analysis on the use of PFTs .
Biological effects of aspirin and clopidogrel in a randomized cross-over study in 96 healthy volunteers.
BACKGROUND Some data suggest that biological ' resistance ' to aspirin or clopidogrel may influence clinical outcome . OBJECTIVE The aim of this study was to evaluate the relationship between aspirin and clopidogrel responsiveness in healthy subjects . METHODS Ninety-six healthy subjects were r and omly assigned to receive a 1-week course of aspirin 100 mg day(-1 ) followed by a 1-week course of clopidogrel ( 300 mg on day 1 , then 75 mg day(-1 ) ) , or the reverse sequence , separated by a 2-week wash-out period . The drug effects were assessed by means of serum TxB2 assay , platelet aggregation tests , and the PFA -100 and Ultegra RPFA -Verify Now methods . RESULTS Only one subject had true aspirin resistance , defined as a serum TxB2 level > 80 pg microL(-1 ) at the end of aspirin administration and confirmed by platelet incubation with aspirin . PFA-100 values were normal in 29 % of the subjects after aspirin intake , despite a drastic reduction in TxB2 production ; these subjects were considered to have aspirin pseudo-resistance . Clopidogrel responsiveness was not related to aspirin pseudo-resistance . Selected polymorphisms of platelet receptor genes were not associated with either aspirin or clopidogrel responsiveness . CONCLUSIONS In healthy subjects , true aspirin resistance is rare and aspirin pseudo-resistance is not related to clopidogrel responsiveness
Results indicated that some PFTs may have some prognostic utility , i.e. a trend for more clinical events to be associated with groups classified as ' aspirin resistant ' .
Study -level effect sizes were generally small and absolute outcome risk was not substantially different between ' aspirin resistant ' and ' aspirin sensitive ' design ations .
Based on assumptions of PFTs being able to accurately identify patients at high risk of clinical events and such patients benefiting from treatment modification , the economic model found that a test-treat strategy was likely to be cost-effective .
However , neither assumption is currently evidence based .
BACKGROUND The use of aspirin is well established for secondary prevention of cardiovascular disease .
However , a proportion of patients suffer repeat cardiovascular events despite being prescribed aspirin treatment .
It is uncertain whether or not this is due to an inherent inability of aspirin to sufficiently modify platelet activity .
This report aims to investigate whether or not insufficient platelet function inhibition by aspirin ( ' aspirin resistance ' ) , as defined using platelet function tests ( PFTs ) , is linked to the occurrence of adverse clinical outcomes , and further , whether or not patients at risk of future adverse clinical events can be identified through PFTs .
OBJECTIVES To review systematic ally the clinical effectiveness and cost-effectiveness evidence regarding the association between PFT design ation of ' aspirin resistance ' and the risk of adverse clinical outcome ( s ) in patients prescribed aspirin therapy .
To undertake exploratory model-based cost-effectiveness analysis on the use of PFTs .