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 .
Aspirin-insensitive thromboxane biosynthesis in essential thrombocythemia is explained by accelerated renewal of the drug target.
Essential thrombocythemia ( ET ) is characterized by enhanced platelet generation and thrombotic complications . Once-daily low-dose aspirin incompletely inhibits platelet thromboxane A(2 ) ( TXA(2 ) ) in the majority of ET patients . In the present study , we investigated the determinants of aspirin-insensitive platelet TXA(2 ) bio synthesis and whether it could be further suppressed by changing the aspirin dose , formulation , or dosing interval . In 41 aspirin-treated ET patients , the immature platelet count predicted serum TXB(2 ) independently of platelet count , age , JAK-2 V617F mutation , or cytoreduction ( β = 3.53 , P = .001 ) . Twenty-one aspirin-treated patients with serum TXB(2 ) ≥ 4 ng/mL at 24 hours after dosing were r and omized to the following 7-day regimens in a crossover design : enteric-coated aspirin 100 mg twice daily , enteric-coated aspirin 200 mg once daily , or plain aspirin 100 mg once daily . A twice-daily regimen caused a further 88 % median ( IQR , 78%-92 % , P < .001 ) TXB(2 ) reduction and normalized the functional platelet response  to  aspirin , as assessed by urinary 11-dehydro-TXB(2 ) excretion and the VerifyNow Aspirin assay . Doubling the aspirin dose reduced serum TXB(2 ) only partially by 39 % median ( IQR , 29%-54 % , P < .05 ) . We conclude that the abnormal megakaryopoiesis characterizing ET accounts for a shorter-lasting antiplatelet effect of low-dose aspirin through faster renewal of platelet cyclooxygenase-1 , and impaired platelet inhibition can be rescued by modulating the aspirin dosing interval rather than the dose
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 .