SPONTANEOUS HOST ENDOTHELIAL GROWTH ON BIOPROSTHETIC VALVES AND ITS RELATION TO CALCIFICATION

We studied host endothelial growth and calcification of bovine pericar dial valve prostheses treated with: (A) 0.625% glutaraldehyde + 4% for maldehyde, (B) 99.5% glycerol or (C) 99.5% glycerol + 4% formaldehyde. Twenty-three stentless chordally supported bileaflet pericardial mitr al valves with treatments A (n = 6), B (n = 6) or C (n = 11) were impl anted in juvenile sheep for 125-273 days. After sacrifice, the anterio r cusp from the annulus to papillary muscle of each valve was examined by scanning electron microscopy for the presence of endothelial cells , and the intrinsic calcification of each valve was determined by meas uring calcium (mug/mg dry weight) from another 1 cm2 piece of grossly normal cusp. Sixty pieces of 1 cm2 pericardium with treatment A, B or C (n = 20 in each group) were implanted in 30 rats for 70 days. Calciu m analysis and histology study of the implants were performed. In shee p, within a similar range of implantation periods, the endothelial gro wth rate of the valves was the highest in group B, 100% (6/6); group C was 45.5% (5/11) and A 16.7% (1/6). There were no significant differe nces in calcium among groups A, B and C. In rat implants, the calcium of group B was much lower than that of A or C (B = 6.92 +/- 4.46 vs A = 144.52 +/- 27.66 or C = 240.54 +/- 13.47, P < 0.05) although its his tology showed more severe degeneration and inflammatory changes. Peric ardial mitral valves treated with glycerol show satisfactory biocompat ibility with regard to host endothelial growth and prevention of calci fication; however, these tissues show evidence of rapid degeneration. Exposure to aldehyde reduces the host endothelial growth on valves and causes calcification. The calcium content in grossly normal areas of the valves does not increase in the groups with less endothelial growt h, although those valves tend to have more calcification, grossly, in some areas. This implies that calcium deposition is not evenly distrib uted in the whole valve; host endothelial growth and calcification are independent of each other in certain areas of valves.