DONOR SHORTAGE - USE OF THE DYSFUNCTIONAL DONOR HEART

The cause of brain death and the physiologic sequelae of brain death m ay impair heart function. Pharmacologic attempts to maintain donor via bility 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 transpl antation with organs donated from infants with sudden infant death syn drome 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 imm ediate peril, we have used donor hearts with documented dysfunction (l eft ventricular shortening fraction [LVSF] < 28%, wall motion abnormal ities, 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 = 1 33, LVSF > 28%). Early death (< 30 days) was similar for the dysfuncti onal donor group (14%) and normal function donor group (11%). Postoper ative inotropic support was equally frequent in both groups. Graft fun ction on echocardiography was normal at 30 days after transplantation for both types of donor organs. We conclude that donor hearts with dec reased left ventricular function (LVSF 15% to 28% and/or asymmetric wa ll motion), despite massive inotropic support, can function normally i n the recipient. Significant donor mitral regurgitation was seen in gr afts that ultimately failed after transplantation. Research into the r eversible mechanisms of myocardial dysfunction associated with brain d eath could enlarge the donor pool.