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 .
The contribution of cyclooxygenase-1 and -2 to persistent thromboxane biosynthesis in aspirin-treated essential thrombocythemia: implications for antiplatelet therapy.
We tested whether cyclooxygenase 2 ( COX-2 ) expression and unacetylated COX-1 in newly formed platelets might contribute to persistent thromboxane ( TX ) bio synthesis in aspirin-treated essential thrombocythemia ( ET ) . Forty-one patients on chronic aspirin ( 100 mg/day ) and 24 healthy subjects were studied .  Platelet COX-2 expression was significantly increased in patients and correlated with thiazole orange-positive platelets ( r = 0.71 , P < .001 ) . The rate of TXA(2 ) bio synthesis in vivo , as reflected by urinary 11-dehydro-TXB(2 ) ( TXM ) excretion , and the maximal biosynthetic capacity of platelets , as reflected by serum TXB(2 ) , were higher in patients compared with aspirin-treated healthy volunteers . Serum TXB(2 ) was significantly reduced by the selective COX-2 inhibitor NS-398 added in vitro . Patients were r and omized to adding the selective COX-2 inhibitor , etoricoxib , or continuing aspirin for 7 days . Etoricoxib significantly reduced by approximately 25 % TXM excretion and serum TXB(2 ) .  Fourteen of the 41 patients were studied again 21 ( + /- 7 ) months after the first visit . Serum TXB(2 ) was consistently reduced by approximately 30 % by adding NS398 in vitro , while it was completely suppressed with 50 microM aspirin . Accelerated platelet regeneration in most aspirin-treated ET patients may explain aspirin-persistent TXA(2 ) bio synthesis through enhanced COX-2 activity and faster renewal of unacetylated COX-1 . These findings may help in reassessing the optimal antiplatelet strategy in ET
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 .