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 recovery of platelet cyclooxygenase activity explains interindividual variability in responsiveness to low-dose aspirin in patients with and without diabetes.
BACKGROUND Interindividual variability in response to aspirin has been popularized as ' resistance ' . We hypothesized that faster recovery of platelet cyclooxygenase-1 activity may explain incomplete thromboxane ( TX ) inhibition during the 24-h dosing interval . OBJECTIVE To characterize the kinetics and determinants of platelet cyclooxygenase-1 recovery in aspirin-treated diabetic and non-diabetic patients . PATIENTS / METHODS One hundred type 2 diabetic and 73 non-diabetic patients on chronic aspirin 100 mg daily were studied .  Serum TXB(2 ) was measured every 3 h , between 12 and 24 h after a witnessed aspirin intake , to characterize the kinetics of platelet cyclooxygenase-1 recovery . Patients with the fastest TXB(2 ) recovery were r and omized to aspirin 100 mg once daily , 200 mg once daily or 100 mg twice daily , for 28 days and TXB(2 ) recovery was reassessed . RESULTS AND CONCLUSIONS Platelet TXB(2 ) production was profoundly suppressed at 12 h in both groups . Serum TXB(2 ) recovered linearly , with a large interindividual variability in slope . Diabetic patients in the third tertile of recovery slopes ( ≥ 0.10 ng mL(-1 ) h(-1 ) ) showed significantly higher mean platelet volume and body mass index , and younger age . Higher body weight was the only independent predictor of a faster recovery in non-diabetics . Aspirin 100 mg twice daily completely reversed the abnormal TXB(2 ) recovery in both groups . Interindividual variability in the recovery of platelet cyclooxygenase activity during the dosing interval may limit the duration of the antiplatelet effect of low-dose aspirin in patients with and without diabetes . Inadequate thromboxane inhibition can be easily measured and corrected by a twice daily regimen
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 .