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

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.