ULTRASTRUCTURAL ANALYSIS OF KEMPERIPLAS-NEO XENOPERICARDIAL PATCH AFTER TRANSANNULAR PATCH REPAIR OF RIGHT VENTRICULAR OUTFLOW TRACT IN PATIENT WITH PULMONARY ATRESIA: 15 YEARS OF FOLLOW-UP

Highlights KemPeriplas-Neo xenopericardial patch, which is used for transannular patch repair at congenital heart disease, undergoes enzymatic degradation 15 years after the implantation. Extracellular matrix delaminates into three layers which respectively consist of fragmented, loose, and dense collagen fibers; however, pericardial patch durability is partially reinforced by neointimal hyperplasia. Disintegration of the collagen fibers are enhanced by natural aging of the xenopericardium, high hemodynamic load, precipitation of circulating collagenases, macrophage infiltration, and weak regeneration. Abstract Aim. To perform an ultrastructural analysis for assessing the remodeling of xenopericardial patch 15 years after transannular repair of right ventricular outflow tract. Methods. KemPeriplas-Neo pericardial patch was explanted 15 years postoperation due to the structural deterioration. The patch was fixed in phosphate-buffered formalin, stained with heavy metals, dehydrated using ethanol and acetone, and impregnated into epoxy resin followed by its polymerization, grinding, polishing, lead citrate counterstaining, and sputter coating. Ultrastructural analysis was performed by backscattered scanning electron microscopy. Results. The explanted patch exhibited extensive remodeling, including the development of a neointima and a tunica adventitia at the luminal and outer surfaces of the patch, respectively. Endothelial cells covering the neointima were elongated along the blood flow. The patch displayed a heterogeneous collagen matrix comprising fragmented, loose, and dense collagen layers. Heterogeneity of collagen fibers and significant macrophage infiltration suggested high proteolytic activity overwhelming the regenerative capacity of fibroblasts, thus indicating ongoing matrix remodeling. The adventitia consisted of loose connective tissue with numerous canonical macrophages and multiple microvessels, indicating active neovascularization. Non-implanted xenopericardial samples demonstrated a uniform collagen fiber architecture without any evidence of enzymatic degradation. Conclusion. Here we provided ultrastructural evidence of long-term biological integration and remodeling of xenopericardial patches after the transannular repair of right ventricular outflow tract. Collagen fragmentation and macrophage infiltration highlighted the complex interplay of enzymatic degradation, hemodynamic stress, immune response, and precipitation of circulating proteases. These findings have critical implications for the design and longevity of next-generation bioprosthetic materials for cardiac surgery.