Donor shortage: use of the dysfunctional donor heart

The cause of brain death and the physiologic sequelae of brain death may impair heart function. Pharmacologic attempts to maintain donor viability may further jeopardize myocardial performance and could only be justified if dysfunctional donor organs subsequently prove to recover normal function after transplantation. Survival data on heart transplantation with organs donated from infants with sudden infant death syndrome indicate that prolonged ischemia (cardiopulmonary resuscitation up to 60 minutes) and metabolic abnormalities a priori do not increase the risk of graft failure. To provide a donor organ to infants in immediate peril, we have used donor hearts with documented dysfunction (left ventricular shortening fraction [LVSF] < 28%, wall motion abnormalities, and mitral regurgitation). The results of heart transplantation with use of dysfunctional donor hearts (n = 22, LVSF = 24.5% +/- 3%) were compared with donors with normal left ventricular function (n = 133, LVSF > 28%). Early death (< 30 days) was similar for the dysfunctional donor group (14%) and normal function donor group (11%). Postoperative inotropic support was equally frequent in both groups. Graft function on echocardiography was normal at 30 days after transplantation for both types of donor organs. We conclude that donor hearts with decreased left ventricular function (LVSF 15% to 28% and/or asymmetric wall motion), despite massive inotropic support, can function normally in the recipient. Significant donor mitral regurgitation was seen in grafts that ultimately failed after transplantation. Research into the reversible mechanisms of myocardial dysfunction associated with brain death could enlarge the donor pool.