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 .
Twice daily dosing of aspirin improves platelet inhibition in whole blood in patients with type 2 diabetes mellitus and micro- or macrovascular complications.
The efficacy of low-dose aspirin in type 2 diabetes mellitus ( T2DM ) has been question ed . We tested if twice daily dosing of aspirin would be more effective in T2DM , possibly due to increased platelet turnover . A r and omised cross-over study compared 75 mg aspirin OD , 75 mg BID and 320 mg OD ( ≥ 2 week treatment periods ) in 25 patients with T2DM and micro- or macrovascular complications . Platelet responses were examined by impedance aggregometry ( WBA ) and the IMPACT-R aspirin  test in whole blood , light transmittance aggregometry in platelet-rich plasma ( LTA ) , and urinary 11-dehydro-thromboxane B2 ( TxM ) . Aspirin 75 mg BID decreased arachidonic acid (AA)-induced WBA compared to 75 mg OD ( 9.7 ± 4.5 vs. 12.6 ± 3.5 ohm ; p = 0.003 ) or to 320 mg OD ( 11.5 ± 4.2 Ohms ; p = 0.049 ) . WBA responses to collagen were similarly attenuated by BID or high dosing ( by 12 - 14 % ; p = 0.02 for both ) . The IMPACT-R showed a better response to 75 mg BID compared to 75 mg OD ( p = 0.049 ) , but not to 320 mg OD . AA-induced aggregation by LTA was < 6.5 % on all occasions , with no differences between aspirin dosages . TxM was reduced after 320 mg OD ( p = 0.002 ) , but not 75 mg BID ( p = 0.07 ) . Reticulated platelets were highly correlated with mean platelet volume ( MPV ; r2 = 0.74 , p<0.0001 ) . Both markers for platelet turnover were correlated with AA-induced WBA , but neither identified patients who benefited from BID dosing dependably . In conclusion , twice daily dosing improved laboratory responses to aspirin in high risk T2DM patients . Studies of whether BID dosing of aspirin can improve clinical outcomes in such patients are of interest
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 .