Issues in monitoring direct thrombin inhibitors: comparison of a new, rapid Ecarin Clotting Time (ECT) test to activated clotting time (ACT) and anti-IIa assays

Abstract number: P1910

Kaldus^* T., Cho† L., Davis^* R., Swan^* H., Lincoff‡ A. M., Moliterno^* D. J., Kottke-Marchant^* K.

‡Cleveland Clinic Foundation, Uruguay ^*Cleveland Clinic Foundation, USA; †Loyola University Medical Center, USA;

Use of direct thrombin inhibitors (DTIs) presents a challenge for monitoring anticoagulant activity, especially with higher doses utilized in the cardiac catheterization laboratory for percutaneous coronary intervention (PCI). It is not well-established whether the activated clotting time (ACT) accurately reflects the anticoagulant effect of DTIs, such as bivalirudin. A new, rapid ECT assay, which provides a specific measure of DTI activity, was compared to two ACT assays and a chromogenic anti-IIa assay in 64 patients receiving bivalirudin ± GP IIb/IIIa antagonist during PCI. Samples were collected at baseline (Sample 1), after DTI bolus (2), after GP IIb/IIIa bolus (3), during the procedure (4) and prior to sheath removal (5). The results in the table show that the bivalirudin concentration (anti-IIa) was stable with time and was not affected by GP IIb/IIIa antagonist administration. The ECT response (sample 2 vs. 1) using both citrate-anticoagulated (8.3-fold increase) and nonanticoagulated specimens (8.5-fold increase) was similar. In contrast, there was only a 2.5-fold increase with the Haemochron ACT and a 3.1-fold increase with the ProDM ACT. The Haemochron ACT showed a further 1.15-fold increase with the GP IIb/IIIa antagonist, but neither the anti-IIa assay, ECT nor ProDM ACT showed an additional change with platelet inhibition. Correlation between the assays for sample 2 was highest between ECT citrated vs. noncitrated (r = 0.79 P < 0.001), but was similarly good between anti-IIa and either citrated ECT (r = 0.72 P < 0.001) or noncitrated ECT (r = 0.58 P < 0.001). There was a weaker correlation between the citrated ECT and either the Haemochron ACT (r = 0.3 p0.0007) or the ProDM ACT (r = 0.53 P < 0.001). Interestingly, the poorest correlation was between the Haemochron ACT and the ProDM ACT (r = 0.18 P = 0.19). These results indicate that the ECT, either using a citrated or noncitrated sample, is a more accurate measure of bivalirudin activity than either the Haemochron or ProDM ACT. The ECT is also not affected by the presence of a GP IIb/IIIa antagonist. These results have implications for guiding anti-coagulation therapy during PCI with DTIs, such as bivalirudin.

Table 1