Abstract
Recent work from this laboratory established feasibility for long-term patency of properly designed valvular xenografts placed without technical fault in the inferior vena cava. Limitations of that work however, included perileaflet fibrosis with reduction of leaflet mobility. The current study evaluates perileaflet thrombosis potentiated by the nonendothelialized leaflet surface as the primary pathogenic mechanism of this problem.
The study includes 18 pericardial xenograft valvular bioprostheses and nine jugular vein valvular autografts placed in the inferior vena cava of 27 dogs All animals received a single bolus of heparin (100u/kg) 5min before vascular clamping. The valves were removed and examined from 1 day to 7.5 months after placement.
In valvular xenografts, perileaflet thrombosis by 1 day progressed to dense fibrosis at 2 months. Despite limitation of leaflet motion, this process caused luminal occlusion in only three valves (83% patency). There were no failures in the nine valvular autografts, with normal valve leaflets and no evidence of thrombus formation as late as 6 months.
Perileaflet thrombosis in pericardial xenograft bioprostheses is a primary event in the ultimate fibrosis of these prosthetic venous valves. Inhibition of thrombosis by the venous endothelial lining may be an explanation for success with the smaller valvular autografts in the same haemodynamic environment.
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