Tissue damage and calcification may be independent mechanisms of bioprosthetic heart valve failure

BACKGROUND AND AIM OF THE STUDY: Porcine bioprosthetic valves have excellent hemodynamics and do not require anticoagulation, but have limited durability. Cusp tearing is a major cause of bioprosthetic valve failure. It has been suggested that the mechanism of bioprosthetic valve failure is stiffening by calcification, which leads to elevated stresses and secondary collagen fiber damage and leaflet tearing. This thesis was tested in explanted porcine bioprostheses. METHODS: A total of 60 explanted porcine bioprosthetic valves was tested mechanically, and 15 explanted valves were examined grossly and histologically. Circumferentially and radially oriented samples of cusp tissue were tested uniaxially in a materials testing machine and compared with five controls. RESULTS: Mean (+/-SD) duration of implantation was 10.9+/-5.6 years. Circumferential specimens from explants were less extensible than controls (11.0+/-5.5% versus 24.5+/-2.8% strain, p <0.001), and failed at lower tensions (973+/-733 versus 3075+/-911 N/m, p = 0.001) and at lower strains (21.2+/-8.1% versus 47.3+/-7.1% strain, p <0.001). Radial specimens from explants were less extensible (28.7+/-6.8% versus 39.2+/-5.9% strain, p = 0.002) and failed at lower strains (60.3+/-17.3% versus 112.2+/-24.9% strain, p <0.001) than the controls. The stiffness of the explants was unchanged from controls in both circumferential and radial samples. There were no differences between explants and controls in radial and circumferential stiffness, and in radial failure strength. Calcification was mild and diffuse in most of the tested samples. Tears were found in areas without calcific deposits, along with breaks in collagen fiber bundles. CONCLUSION: These results do not support the thesis that calcification stiffens glutaraldehyde-fixed porcine bioprostheses, except when the entire cusp is transformed into a solid mass of mineral. Rather, leaflet tears may develop as a result of accumulated mechanical damage that is independent of calcification.