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Blood, 6 August 2009, Vol. 114, No. 6, pp. 1276-1279.
Prepublished online as a Blood First Edition Paper on May 12, 2009; DOI 10.1182/blood-2009-03-209981.


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VASCULAR BIOLOGY

Brief report

Valves of the deep venous system: an overlooked risk factor

Erin G. Brooks1,*, Winifred Trotman1,*, Marilyn P. Wadsworth1, Douglas J. Taatjes1, Mark F. Evans1, Frank P. Ittleman2, Peter W. Callas3, Charles T. Esmon4, and Edwin G. Bovill1

Departments of 1 Pathology, 2 Surgery/Thoracic-Cardiovascular, and 3 Mathematics/Statistics, University of Vermont, Burlington; and 4 The Howard Hughes Medical Institute, Oklahoma Medical Research Foundation, Oklahoma City

Deep venous valves are frequent sites of deep venous thrombosis initiation. However, the possible contribution of the valvular sinus endothelium has received little attention in studies of thrombosis risk. We hypothesized that the endothelium of valve sinus differs from that of vein lumen with up-regulation of anticoagulant and down-regulation of procoagulant activities in response to the local environment. In pursuit of this hypothesis, we quantified endothelial protein C receptor (EPCR), thrombomodulin (TM), and von Willebrand factor (VWF) by immunofluorescence in great saphenous veins harvested at cardiac bypass surgery. We found significantly increased expression of EPCR and TM in the valvular sinus endothelium as opposed to the vein lumenal endothelium, and the opposite pattern with VWF (paired t test for TM and EPCR, each P < .001; for VWF, P = .01). These data support our hypothesis and suggest that variation in valvular sinus thromboresistance may be an important factor in venous thrombogenesis.


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