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 .
Increased protein glycation in diabetes mellitus is associated with decreased aspirin-mediated protein acetylation and reduced sensitivity of blood platelets to aspirin
Reduced effectiveness of the most common antiplatelet drug , acetylsalicylic acid ( ASA , aspirin ) , in diabetes mellitus has been associated with a lowered platelet sensitivity to ASA and related to glycemic control in diabetic patients . Our objectives were ( a ) to monitor the chemical background of how chronic hyperglycemia affects platelet response to ASA in diabetes and ( b ) to study a chemical competition between the amount of bound acetyl residues and the extent of protein glycation in blood platelets . Using whole-blood impedance aggregometry and platelet function analyzer ( PFA-100 ) we observed a reduced platelet response to ASA in diabetic patients ( 14 % vs. 79 % for PFA-100 collagen-epinephrine occlusion time ) and an association between the index of glycemic control and platelet refractoriness to ASA ( rS=−0.378 ) . Impaired platelet response to ASA was related to enhanced platelet protein glycation ( 3.6±0.4 in diabetes vs. 2.3±0.4 µmol fructosamine/µg protein in control ) and reduced incorporation of acetyl residue into proteins of platelets from diabetic patients ( 47.4±2.0 in control vs. 33.1±0.7 µmol acetyl/µg protein in diabetic subjects ) . Incubation of blood platelets with increasing concentrations of glucose and ASA under in vitro conditions led to excessive modification in protein amino groups : glucose and ASA competed with each other in the course of nonenzymatic modifications , glycosylation , or acetylation , and their contributions to the occupancy of protein amino groups ( R2=0.22 for glucose , R2=0.43 for ASA ) were dependent upon the concentrations of glucose and ASA . Overall the effects of high glucose and high ASA on the overall occupancy of protein free amino groups are not additive . While at higher concentrations ASA overcomes the effects of hyperglycemia and retards glycation , high glucose makes acetylation less efficient , and therefore the result ant chemical modification becomes greatly reduced . In conclusion , diminished susceptibility of various platelet proteins and receptors on blood platelet membranes to acetylation and high ambient glucose might underlie the apparently differentiated sensitivity of blood platelets to ASA and determine platelet “ insensitivity to aspirin ” in diabetic
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 .