(203) Two 10-Gene Modified Xenoheart Transplants into Brain Dead Decedents

PurposeThe dearth of donor hearts for allotransplantation has led to the development of genetically modified porcine xenografts. To date, only one xenoheart has been implanted into a living human recipient. We report the findings of 2 xenoheart transplants into brain dead human decedents.MethodsTwo 10-gene porcine xenografts were transplanted into brain-dead decedents and monitored over 66 hours each. Transjugular biopsies at 24 hours, 48 hours, and explant were evaluated for ACR and AMR.ResultsIn the first decedent, a rising lactate from inadequate tissue perfusion due to an undersized donor heart (70-kg pig) for a male recipient (82 kg, 179 cm) led to increasing vasopressor requirements after the first 24 hours and multi-organ system failure. The second decedent demonstrated clinical stability, though the recipient had received an allotransplant years before that failed pre-xenotransplant requiring CRRT. Biopsies at 24 and 48 hours showed no evidence of ACR or AMR. Explant demonstrated patchy subendocardial hemorrhage (Figure 1) likely from mild preservation injury. Histologically, the hearts showed sparse lymphocytic inflammation not associated with myocyte injury. At explant, ACR was graded as 1R and no AMR appreciated. (Figure 2)ConclusionBoth xenografts demonstrated normal biventricular function over the study period. In the first decedent, late decline in cardiac function was likely due to a size discrepancy between xenograft and recipient. There was minimal histologic evidence of ACR and no evidence of AMR. Future studies with longer follow up will be important. The dearth of donor hearts for allotransplantation has led to the development of genetically modified porcine xenografts. To date, only one xenoheart has been implanted into a living human recipient. We report the findings of 2 xenoheart transplants into brain dead human decedents. Two 10-gene porcine xenografts were transplanted into brain-dead decedents and monitored over 66 hours each. Transjugular biopsies at 24 hours, 48 hours, and explant were evaluated for ACR and AMR. In the first decedent, a rising lactate from inadequate tissue perfusion due to an undersized donor heart (70-kg pig) for a male recipient (82 kg, 179 cm) led to increasing vasopressor requirements after the first 24 hours and multi-organ system failure. The second decedent demonstrated clinical stability, though the recipient had received an allotransplant years before that failed pre-xenotransplant requiring CRRT. Biopsies at 24 and 48 hours showed no evidence of ACR or AMR. Explant demonstrated patchy subendocardial hemorrhage (Figure 1) likely from mild preservation injury. Histologically, the hearts showed sparse lymphocytic inflammation not associated with myocyte injury. At explant, ACR was graded as 1R and no AMR appreciated. (Figure 2) Both xenografts demonstrated normal biventricular function over the study period. In the first decedent, late decline in cardiac function was likely due to a size discrepancy between xenograft and recipient. There was minimal histologic evidence of ACR and no evidence of AMR. Future studies with longer follow up will be important.