Hemostasis in the era of the chronic anticoagulated patient

The principal goal of this article is to develop an understanding of how poly-N-acetylglucosamine (pGlcNAc) helps to achieve hemostasis through mechanisms that involve vasoconstriction, red blood cell agglutination and platelet activation for fibrin clot formation. Several important features of these three mechanisms should be understood. The involvement of endothelin-1 in mediating vasoconstriction should be recognized, as well as the observation that red blood cell agglutination is mediated by direct contact of the cells with pGlcNAc fibers. Also, the ability of pGlcNAc to contact activate platelets through integrin-dependent mechanisms and the resulting ability of the platelet to activate thrombin for fibrin gel formation should be understood. It is also important to recognize that having three redundant (and synergistic) mechanisms for surface hemostasis with pGlcNAc imparts utility when patients have specific bleeding diapathies due to anticoagulation therapies, hemophilia, etc. It should also be realized that the hemostatic properties of pGlcNAc are dependent on the specific structure of the polymer as well as the small (fine) diameter of the polymer fibers. Finally, it is important to understand that the acceleration of hemostasis at the dermal opening of a track will accelerate fibrin clot formation in the entire track, because Virchow s three conditions for thrombus formation are satisfied: hypercoagulability (provided by the hemostatic mechanisms of the pGlcNAc), stagnant blood (when a clot forms on the surface of the pGlcNAc) and tissue damage from the procedure.