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Immunosuppression The goal of immunosuppressive therapy is to prevent rejection while minimizing morbidities related to chronic immune suppression There are a large number of center-specific protocols for the maintenance immunosuppression, with ongoing controversy regarding the optimal regime (Figs 67.17 and 67.18) Indeed, there are a myriad of agents, dosages, protocols, and combinations that have been used for both the induction and maintenance of immunosuppression, making definitive comparisons and recommendations difficult.2 A detailed discussion of the various protocols is beyond the scope of this chapter FIG 67.17 Summary of maintenance immunosuppression in children after heart transplant at the time of hospital discharge by era MMF, Mycophenolate mofetil; MPA, mycophenolic acid (From the registry of the International Society of Heart and Lung Transplantation J Heart Lung Transplant 2016;35(10):1185–1195.) FIG 67.18 Summary of maintenance immunosuppression in children at 1 and 5 years after heart transplantation AZA, Azathioprine; MMF, mycophenolate mofetil; MPA, mycophenolic acid (From the registry of the International Society of Heart and Lung Transplantation J Heart Lung Transplant 2016;35(10):1185–1195.) Monitoring and Surveillance After Transplantation The hallmark of care subsequent to transplantation is meticulous attention to detail, with a high index of suspicion for transplant-related problems Care of children after heart transplantation must account for physical growth and development; the stage of immunologic development; intellectual, emotional, and social maturation; educational activities; and other parameters of quality of life Each one of these aspects can significantly affect morbidity and mortality after transplantation Rejection Rejection is the process of destruction of genetically foreign material by the immune system of the host It varies in severity and timing between individuals and may wax and wane within an individual patient Acute rejection remains an important cause of mortality and morbidity after transplantation (see Table 67.3 and Fig 67.14), although its incidence has decreased in the most recent era (Fig 67.19) There are few identifiable risk factors for rejection prior to transplantation other than sensitization to HLA antigens (see earlier) Preformed donor-specific anti-HLA antibodies can lead to antibody-mediated rejection (AMR) within the first few hours after transplantation Cellular rejection usually starts during the first few weeks and is present to some degree in most patients Rejection is most commonly mediated by T cells, although humoral rejection mediated by B-cell activation is increasing owing to the larger number of patients sensitized to HLA antigens There is increasing evidence for the role of both acute cellular rejection (ACR) and AMR in the survival of the transplanted organ (Fig 67.20) and the development of vasculopathy.2,12,61,62