Potentiation of thrombus instability: a contributory mechanism to the effectiveness of antithrombotic medications

Figures

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  Fig. 1. Influences determining arterial thrombus stability, under high shear conditions. The strength of the attachment to the vessel wall and the tightness of the platelet core determine its ability to resist disruption by high shear forces and fibrinolysis. Medications that impact on thrombus stability are shown on left, NOAC non vitamin K oral anticoagulant

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  Fig. 2. Key platelet and plasma proteins contributing to thrombus stability. I Platelet receptors and ligands involved in initial integrina IIbb3 activation and reversible platelet aggregation. The absence of these molecules increases thrombus instability. Also indicated is a box with intracellular signalling proteins controlling this process. II Contact-dependent signalling mechanisms implicated in platelet contraction and irreversible platelet aggregation. Fibrin formed by the coagulation process stabilizes the platelet aggregate. III Plasma coagulation factors, via the intrinsic (factor XII, FXII) and extrinsic (tissue factor, TF) pathways, mediating platelet-dependent thrombin and fibrin generation, stabilizing a growing thrombus. Also indicated is a primary mechanism of platelet-leucocyte interaction via P-selectin and PSGL-1. Reproduced with permission from Cosemans et al. [14]