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 .
Incomplete Inhibition of Thromboxane Biosynthesis by Acetylsalicylic Acid: Determinants and Effect on Cardiovascular Risk
Background — Incomplete inhibition of platelet thromboxane generation , as measured by elevated urinary 11-dehydro thromboxane B2 concentrations , has been associated with an increased risk of cardiovascular events . We aim ed to determine the external validity of this association in  aspirin-treated patients enrolled in the Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization , Management and Avoidance ( CHARISMA ) trial and to determine whether there are any modifiable factors or interventions that lower urinary 11-dehydro thromboxane B2 concentrations that could thereby reduce cardiovascular risk . Methods and Results — Urinary 11-dehydro thromboxane B2 concentrations were measured in 3261 aspirin-treated patients at least 1 month after they had been r and omly assigned to placebo or clopidogrel .  Baseline urinary 11-dehydro thromboxane B2 concentrations in the highest quartile were associated with an increased risk of stroke , myocardial infa rct ion , or cardiovascular death compared with the lowest quartile ( adjusted hazard ratio 1.66 , 95 % CI 1.06 to 2.61 , P=0.03 ) . Increasing age , female sex , history of peripheral artery disease , current smoking , and oral hypoglycemic or angiotensin-converting enzyme inhibitor therapy were independently associated with higher urinary concentrations of 11-dehydro thromboxane B2 , whereas aspirin dose ≥150 mg/d , history of treatment with nonsteroidal antiinflammatory drugs , history of hypercholesterolemia , and statin treatment were associated with lower concentrations . R and omization to clopidogrel ( versus placebo ) did not reduce the hazard of cardiovascular events in patients in the highest quartile of urinary 11-dehydro thromboxane B2 levels . Conclusions —  In aspirin-treated patients , urinary concentrations of 11-dehydro thromboxane B2 are an externally valid and potentially modifiable determinant of stroke , myocardial infa rct ion , or cardiovascular death in patients at risk for atherothrombotic events
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 .