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 .
Measuring aspirin resistance, clopidogrel responsiveness, and postprocedural markers of myonecrosis in patients undergoing percutaneous coronary intervention.
Aspirin and clopidogrel are proven to prevent thromboembolic events during percutaneous coronary intervention ( PCI ) . Enzyme release of creatine kinase-MB ( CK-MB ) enzyme during PCI has been associated with an increased risk of future adverse cardiac events . This study examined the correlation between measurements of aspirin resistance and the level of inhibition of the thienopyridine-specific P2Y12 platelet receptor and CK-MB release after PCI . We prospect ively studied 330 patients with elective PCI treated with drug-eluting stents . Patients were pretreated with aspirin and clopidogrel . Patients with positive CK-MB or acute coronary syndrome and those on glycoprotein IIb/IIIa inhibitors were excluded .  Serum assays of aspirin resistance  ( Ultegra Rapid Platelet Function Assay-ASA , Accumetrics ) and  clopidogrel resistance  ( Rapid Platelet Function Assay P2Y12 , Accumetrics ) were performed before PCI . Serum troponinI and CK-MB levels were measured at 8 , 16 , and 24 hours after PCI . Aspirin resistance unit ( ARU ) measurement > or = 550 was detected in 12 patients ( 3.7 % ) . Mean platelet reactivity unit ( PRU ; measurement of inhibition of P2Y12 activity ) was 192.2 + /- 95.4 ( lower PRU , more inhibition of P2Y12 receptor ) . There was no correlation between level of ARU or PRU and troponin I or CK-MB release after PCI at any time point . Only multivessel coronary disease was found to be a predictor of any increase in CK-MB in a multivariate analysis ( odds ratio 2.2 , 95 % confidence interval 1.4 to 3.3 , p = 0.0003 ) . A positive correlation was found between levels of ARU and PRU . Target vessel revascularization/major adverse cardiac event rate at 6 months was 8.2 % with no correlation between ARU or PRU and release of cardiac enzymes or occurrence of adverse cardiac events . In conclusion , this study does not support routine measurements of aspirin and clopidogrel resistance in stable patients undergoing PCI
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 .