Mediastinitis-Associated Immune Activation as a Potential Accelerator of Xenograft Inflammatory Response

Bovine jugular vein graft is widely used for right ventricular outflow tract reconstruction in congenital heart disease, with a reported median time to conduit exchange exceeding 5 years in infants. The impact of severe postoperative infection on immune-mediated xenograft failure remains incompletely characterized.

A 23-month-old boy with tetralogy of Fallot presented with critical obstruction of the distal pulmonary trunk 5 months after right ventricular outflow tract reconstruction with a 14-mm bovine jugular vein conduit. His postoperative course had been complicated by mediastinitis, which was successfully treated. Despite transcatheter intervention, progressive conduit distal stenosis ultimately required surgical reintervention. The explanted xenograft showed multinucleated giant cells, marked fibrosis, and extensive collagen degradation, consistent with an intense foreign-body inflammatory reaction. Following replacement with a 14-mm valved expanded polytetrafluoroethylene conduit, hemodynamics improved and remained stable on follow-up.

We discuss the possible role of postoperative Staphylococcus epidermidis mediastinitis in accelerating xenograft degeneration through immune activation. Close surveillance of xenograft function and consideration of alternative conduits made of biologically inert materials may be warranted in high-risk settings.

Mediastinitis may function as an immunologically mediated trigger, potentially accelerating xenograft degeneration. For patients at an increased risk of inflammatory or infectious complications, expanded polytetrafluoroethylene conduits may represent a reasonable alternative.