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Graft, Vol. 5, No. 4, 212-222 (2002)
© 2002 SAGE Publications

Prothrombogenic Microvasculature and Transplant Outcome

Carlos A. Labarrere

Methodist Research Institute, Clarian Health

David R. Nelson

Methodist Research Institute, Clarian Health

Steven J. Miller

Methodist Research Institute, Clarian Health

A major obstacle to the long-term success of transplanted solid organs is the developmentof transplant-associated vasculopathy. A prime risk factor for the development ofvascular disease is the conversion of the microvasculature from a thromboresistant to aprothrombogenic state, leading to fibrin deposition. A thromboresistant microvasculatureis characterized by vessels in which the endothelium has intact natural anticoagulantand fibrinolytic pathways and by the lack of activated endothelial cells. A prothrombogenicmicrovasculature results when there are failures in anticoagulantpathways, such as the protein C and the vascular antithrombin pathways, or when thereis an absence of fibrinolytic activity, as when tissue plasminogen activator is depleted.Activated endothelium, characterized by increased arterial expression of moieties suchas intercellular adhesion molecule-1 and human leukocyte antigen-DR, also is associatedwith a prothrombogenic microvasculature. The presence of a prothrombogenic microvasculatureearly after transplantation is associated with an increased incidence ofboth coronary artery disease and chronic graft failure. Although the mechanisms responsiblefor the loss of thromboresistant endothelium are unclear, the fact that changesin the anticoagulant, fibrinolytic, and activational status of endothelial cells may occurearly after transplantation suggests a peritransplant phenomenon as an initiating event.The use of both new and established therapies to inhibit the formation of a prothrombogenicmicrovasculature could slow the development of transplant coronary artery diseaseand significantly improve allograft survival.

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