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 .
Heterogeneity in platelet cyclooxygenase inhibition by aspirin in coronary artery disease.
BACKGROUND Platelets , long believed to be incapable of de novo protein synthesis , may retain their ability to form the cyclooxygenase ( COX ) enzyme once it has been inactivated by aspirin . This may explain the inefficacy of the drug to induce sustained platelet inhibition in certain patients . We evaluated the stability of platelet inhibition following once-daily enteric-coated aspirin administration . METHODS Platelet responsiveness to aspirin was evaluated in 11 stable coronary artery disease patients on chronic aspirin therapy before and 1 , 3 , 8 , and 24h after observed ingestion of 80-mg enteric-coated aspirin . Inhibition of the COX pathway was measured pharmacologically through plasma thromboxane ( Tx ) B(2 ) levels , and functionally by light transmission aggregometry in response to arachidonic acid . COX-independent platelet activity was measured in response to adenosine diphosphate , epinephrine and collagen . RESULTS Plasma TxB(2 ) levels showed profound inhibition of TxA(2 ) formation , which was stable throughout 24h , in all but 1 subject . This subject had optimal response to aspirin ( inhibition of platelet TxA(2 ) production within 1h ) , but recovered the ability to synthesize TxA(2 ) within 24h of aspirin ingestion . Arachidonic acid-induced platelet aggregation closely mirrored TxB(2 ) formation in this patient , portraying a functional ability of the platelet to aggregate within 24h of aspirin ingestion . COX-independent platelet aggregation triggered TxA(2 ) production to a similar extent in all patients , likely through signal-dependent protein synthesis . CONCLUSIONS COX-dependent platelet activity is recovered in certain individuals within 24h of aspirin administration . Further research should consider increasing aspirin dosing frequency to twice daily , to allow sustained inhibition in such subjects
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 .