Explanted bioprosthetic valves with structural degeneration exhibited oxidized LDL, macrophage infiltration, and active MMP-9 in 13 of 18 cases, whereas nonimplanted controls showed no such evidence.
Observational (n=22)
Are lipid-mediated inflammatory mechanisms involved in the structural valve degeneration of bioprostheses?
Lipid-mediated inflammation, characterized by ox-LDL and macrophage infiltration, may contribute to structural valve degeneration in bioprostheses, suggesting a potential role for atherosclerotic risk factor modification.
Absolute Event Rate: 72.2% vs 0%
BACKGROUND: The durability of bioprosthetic valves is limited by structural valve degeneration (SVD) leading to bioprostheses (BPs) stenosis or regurgitation. We hypothesized that a lipid-mediated inflammatory mechanism is involved in the SVD of BPs. MATERIAL AND METHODS: Eighteen Freestyle stentless BP valves were explanted for SVD at a mean time of 5.9 +/- 3 years after implantation and were analysed by immunohistochemistry and transmission electron microscopy (TEM). RESULTS: The mean age of the patients was 65 +/- 8 years and there were 11 male and seven female patients. Two of the 18 BPs had macroscopic calcification, whereas the other valves had minimal or no macroscopic calcification. Tears at the commissures leading to regurgitation was present in 16 BPs. Immunohistochemistry showed the presence of oxidized low-density lipoprotein (ox-LDL) and glycosaminoglycans in the fibrosa layer of 13 BPs. Areas with ox-LDL were infiltrated by macrophages (CD68(+)) co-expressing the scavenger receptor CD36 and metalloproteinase-9 (MMP-9). Zymogram showed the active form of MMP-9 within explanted BPs. EM studies revealed the presence of lipid-laden cells featuring foam cells and fragmented collagen. Nonimplanted control BPs obtained from the manufacturer (n = 4) had no evidence of lipid accumulation, inflammatory cell infiltration or expression of MMP9 within the leaflets. CONCLUSIONS: These results support the concept that lipid-mediated inflammatory mechanisms may contribute to the SVD of BPs. These findings suggest that modification of atherosclerotic risk factors with the use of behavioural or pharmacological interventions could help to reduce the incidence of SVD.
Shetty et al. (Wed,) conducted a observational in Structural valve degeneration of bioprostheses (n=22). Explanted Freestyle stentless bioprosthetic valves vs. Nonimplanted control bioprostheses was evaluated on Presence of oxidized low-density lipoprotein (ox-LDL) and glycosaminoglycans in the fibrosa layer. Explanted bioprosthetic valves with structural degeneration exhibited oxidized LDL, macrophage infiltration, and active MMP-9 in 13 of 18 cases, whereas nonimplanted controls showed no such evidence.