Differential thrombogenicity of artery and vein: the role of von Willebrand factor.

There exists clinical evidence for a difference in the relative thrombogenicity of arterial and venous surfaces. We studied this phenomenon in an in vitro model where the effects of hemodynamic differences could be controlled. Nonanticoagulated human blood was perfused across injured (air-insufflated) arterial and venous surfaces in a recirculating perfusion system at shear rates of 500 and 1500/sec. Thrombus formation was assessed by measuring radiolabeled platelet (111In) and fibrin (125I) deposition on the surfaces. The role of von Willebrand factor (vWF) in arterial and venous thrombosis was evaluated by blocking its effect with polyclonal anti-vWF antibody (vWF Ab). Raw data were converted to log10 for statistical analysis. The increased thrombogenicity of injured venous vs. arterial segments was confirmed by these studies (p < 0.001). The addition of vWF Ab decreased platelet and fibrin deposition (p < 0.001) and these effects were greater in veins than in arteries. The difference in platelet deposition between arteries and veins was more pronounced at lower shear rates (p < 0.05), an effect not observed with fibrin deposition. To determine whether the increased thrombogenicity of veins could be explained by an increased content of subendothelial vWF, the amount of vWF was assessed by incubating injured vessels with 125I vWF Ab and then measuring the radioactivity of the vessels. Veins had a higher content of vWF than arteries, as implied by the higher amount of radiolabeled vWF Ab (813 +/- 90 in veins vs. 2173 +/- 317 in arteries, p < 0.001). These observations suggest that increased thrombogenicity of veins may in part be explained by intrinsic differences in subendothelial vWF and subsequent platelet attachment.