Outcomes of heart transplantation using donor hearts from infants with sudden infant death syndrome
ABSTRACT Uncertainty exists whether hearts from infants who have died of sudden infant death syndrome (SIDS) are acceptable for transplantation because the mechanism of death in SIDS remains unclear. We analyzed post-transplant outcomes in infants who received a heart from a donor where SIDS was the primary cause of brain death.
This retrospective multicenter cohort study used data from the Organ Procurement and Transplant Network (OPTN). All infants aged < 12 months undergoing heart transplant between 1994 and 2008 were included. A Cox proportional hazards model was used to determine whether donor SIDS was independently associated with post-transplant graft loss (death or retransplant).
During the study period, 66 of 1033 infants (6.4%) who underwent heart transplant received an allograft from a SIDS donor. These infants were similar to the remaining infants with respect to age, diagnosis, blood type, and invasive support. In multivariable analysis, graft loss was associated with congenital heart disease (hazard ratio [HR], 1.6; 95% confidence interval [CI], 1.2-2.1), ventilator (HR, 1.4; 95% CI, 1.1-1.9), and extracorporeal membrane oxygenation support (HR, 3.0; 95% CI, 2.2-4.3), but not donor SIDS (HR, 1.0; 95% CI, 0.6-1.5), suggesting graft survival in SIDS-donor heart recipients was similar to the remaining infants. Primary causes of post-transplant death in infants receiving SIDS-donor hearts and the remaining infants were similar.
Graft survival was similar in infants who received SIDS-donor hearts compared with those who received hearts from donors who died of other causes. There was no increase in incidence of non-rejection-related cardiac deaths after transplant in these children.
Chapter: Coronary Heart Disease[Show abstract] [Hide abstract]
ABSTRACT: The heart is a dynamic organ that pumps more than two billion beats in the average lifetime. It is the first organ to develop during embryogenesis and requires a complex interaction of signaling factors, transcriptional networks, and microRNAs to regulate discrete stages of cardiac specification, differentiation, chamber formation, and growth. Spontaneous genetic mutations in humans and engineered molecular mutations in model systems have improved our understanding of cardiac development in both the human and nonprimate heart. While congenital heart disease (CHD) is relatively common and can be life-threatening, emerging therapies including catheter-based interventions, surgical repair, cellular repair, and cell therapy are improving survival and resulting in increased numbers of adults living with heart disease. Better understanding the mechanisms that govern cardiac development can clarify the pathology of CHD and help develop new therapies for this patient population.Coronary Heart Disease, 01/2012: pages 19-42; , ISBN: 978-1-4614-1474-2