Spontaneous host endothelial growth on bioprosthetic valves and its relation to calcification

We studied host endotbelial growth and calcification of bovine pericardial valve prostheses treated with: (A) 0.625% glutaraldehyde + 4% formaldehyde, (B) 99.5% glycerol or (C) 99.5% glycerol + 4% formaldehyde. Twenty three stentless chordally supported bileaflet pericardial mitral valves with treatments A (n = 6), B (n = 6) or C (n = 11) were implanted in juvenile sheep for 125-273 days. After sacrifice, the anterior 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 measuring calcium (pg/mg dry weight) from another 1 cm* 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. Calcium analysis and histology study of the implants were performed. In sheep, within a similar range of implantation periods, the endothelial growth rate of the valves was the highest in group B, 100% (6/6); group C was 45.5% (5/11) and A 16.7% (l/6). There were no significant differences 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 f 13.47, P 0.05) although its histology showed more severe degeneration and inflammatory changes. Pericardial mitral valves treated with glycerol show satisfactory biocompatibility with regard to host endothelial growth and prevention of calciflcation; however, these tissues show evidence of rapid degeneration. Exposure to aldehyde reduces the host endothelial growth on valves and causes calcitication. The calcium content in grossly normal areas of the valves does not increase in the groups with less endothelial growth, although those valves tend to have more calcification, grossly, in some areas. This implies that calcium deposition is not evenly distributed in the whole valve; host endothelial growth and calcification are independent of each other in certain areas of valves. (Eur J Cardio-thorac Surg (1993) 7:591-5961.