Antiplatelet Treatment Does Not Affect the Kinetics of Clot Formation After TF Pathway Activation in Patients with Carotid Artery Disease. A Thromboelastography Study

Abstract number: P2197

Kostantinidis K, Gerasimidis T

Background:  Antiplatelet treatment is the cornerstone of secondary antithrombotic prophylaxis. Platelet adhesion is one of the first steps of thrombogenesis. Tissue factor (blood-born or at the ruptured atheromatic plaque) is the major trigger for thrombin generation, which results in platelet activation and thrombus formation. Thrombin activated platelets contribute to the amplification of thrombin generation and clot growth.

Aim:  We investigated the influence of antiplatelet treatment on the dynamics of clot formation in whole blood (WB) after TF-pathway activation using a WB-TF-Thromboelastography (WB-TF-TEG) assay, as previously described (Gerotziafas et al., Thromb Haemost 2004;92:1296–302).

Patients and methods:  Citrated WB was collected from 20 patients with carotid artery disease, treated with antiplatelet agents (aspirin and/or clopidogrel) and from 20 normal subjects. The WB-TF-TEG was performed within 30–90 minutes after blood sampling on a computerized thromboelastograph ROTEM^® (PENTAPHARM, Munich, Germany). Coagulation was triggered by addition of CaCl₂ (0.2 mM) and rTF (Innovin Dade Behring, Germany) diluted 1/8000 in plasma. Four parameters were analyzed: Clotting Time (CT); Clot Formation Time (CFT), time required to reach a fixed level (20 mm) of clot firmness; alpha angle (a) reflecting clot development kinetics, and Maximum Clot Firmness (MCF).

Results:  Antiplatelet treatment did not modify the WB-TF-TEG profile as compared to the control group. Control (n= 20): CT: 309 ± 48, CFT: 89 ± 16, a-angle: 73 ± 3, MCF: 69 ± 10. Baseline patients: CT: 282 ± 52, CFT: 89 ± 25, a-angle: 72 ± 4, MCF: 66 ± 5 (In all cases control vs baseline P > 0.05).

Conclusion:  These data indicate that when thrombin generation is triggered by TF pathway activation in WB, the antiplatelet treatment does not modify the kinetics of thrombus formation neither its physical characteristics. Probably the inhibition of platelet ADP and/or arachidonic acid pathways is not sufficient to modify the kinetics of clot formation and its physical characteristics when thrombin is generated. The physiological relevance of this observation is studied.