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 .
Association of recurrent cerebral infarction with adenosine diphosphate- and collagen-induced platelet aggregation in patients treated with ticlopidine and/or aspirin.
Although the platelet aggregation test is the most common method for evaluating response to antiplatelet therapy , little is known about the association of recurrent cerebral infa rct ion with platelet aggregation in the presence of various different antiplatelet drugs . We prospect ively evaluated adenosine diphosphate (ADP)- and collagen-induced platelet aggregation and followed the incidence of recurrent infa rct ion in patients categorized into 3 groups based on treatment ; aspirin ( n = 144 ) , ticlopidine ( n = 100 ) , and aspirin + ticlopidine ( n = 96 ) . The patients in each treatment group were stratified into quartiles according to platelet aggregation , and the association of recurrent infa rct ion with platelet aggregation was investigated . ADP-induced platelet aggregation values were significantly lower in the ticlopidine group and the aspirin + ticlopidine group compared with the aspirin group ( P < .001 ) , and collagen-induced platelet aggregation values were significantly lower in the aspirin group and the aspirin + ticlopidine group compared with the ticlopidine group ( P < .001 ) . In the aspirin group , the recurrence rate was somewhat higher in the higher aggregation quartiles than in the lower aggregation quartiles of 2 μg/mL collagen , the differences were not statistically significantly ( P = .243 ) . In the ticlopidine group , the recurrence rate was significantly higher in the lower aggregation quartiles compared with the higher aggregation quartiles of 1 μmol/L ADP ( P = .025 ) . No tendencies were found in the aspirin + ticlopidine group . Although the study is limited by its small sample size , the results suggest a possible difference between aspirin therapy and ticlopidine therapy in the pattern of association of recurrent infa rct ion with platelet aggregation
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 .