Assessment of platelet-derived thrombogenicity with the total thrombus-formation analysis system in coronary artery disease patients receiving antiplatelet therapy.

2016 
Essentials Total thrombus-formation analysis system (T-TAS) quantitatively measures platelet thrombus formation. We examined the utility of T-TAS in patients with coronary artery disease. T-TAS can discriminate different types of the antiplatelet therapy in the same measuring method. Genetic background, cytochrome P-450 2C19 genotypes, also influenced T-TAS parameters. Summary Background Accurate evaluation of thrombogenicity helps to prevent thrombosis and excessive bleeding. The total thrombus-formation analysis system (T-TAS) was developed for quantitative analysis of platelet thrombus formation by the use of microchips with thrombogenic surfaces (collagen, platelet chip [PL-chip]; collagen plus tissue factor, atherome chip [AR-chip]). We examined the utility of the T-TAS in the assessment of the efficacy of antiplatelet therapy in patients with coronary artery disease (CAD). Methods and Results In this cross-sectional study, 372 consecutive patients admitted to the cardiovascular department were divided into three groups: patients not receiving any antiplatelet therapy (control, n = 56), patients receiving aspirin only (n = 69), and patients receiving aspirin and clopidogrel (n = 149). Blood samples were used for the T-TAS to measure the platelet thrombus-formation area under the curve (AUC) at various shear rates (1500 s−1 [PL18-AUC10] and 2000 s−1 [PL24-AUC10] for the PL-chip; 300 s−1 [AR10-AUC30] for the AR-chip). The on-clopidogrel platelet aggregation was measured by the use of P2Y12 reaction units (PRUs) with the VerifyNow system. The mean PL24-AUC10 levels were 358 ± 111 (± standard deviation) (95% confidence interval [CI] 328.9–387.1) in the control group, 256 ± 108 (95% CI 230.5–281.5) in the aspirin group, and 113 ± 91 (95% CI 98.4–127.6) in the aspirin/clopidogrel group. In the aspirin/clopidogrel group, the PL24-AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 ± 112, 95% CI 103.4–200.6) than in the non-PM group (87 ± 74, 95% CI 73.8–100.2). Conclusions Our findings suggest that the PL24-AUC10 level measured by the T-TAS is a potentially suitable index for the assessment of antiplatelet therapy in CAD patients.
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