Cardiac iron overload following liver transplantation in patients without hereditary hemochromatosis or severe hepatic iron deposition.

Abstract

Cardiac iron overload following liver transplantation in patients without hemochromatosis but with severe hepatic iron deposition has been reported to result in heart failure and/or death in case reports and small case series. However, the frequency and causes of cardiac iron overload following liver transplantation and its relationship to cardiac dysfunction in patients without severe hepatic iron deposition are unclear. The primary inclusion criteria for this study were liver transplantation followed by autopsy or cardiac transplantation within 1 year. Cases of known hemochromatosis were excluded. Iron stains were performed on left ventricular myocardium from either the autopsy or surgically resected heart, as well as the surgically resected liver. Nineteen cases met the study criteria: 18 autopsies and 1 case of cardiac transplantation. None of the resected livers evaluated showed severe iron deposition. Myocardial iron deposition was identified in 7 (37%) of the cases. The presence of myocardial iron deposition was not significantly associated with the grade of hepatic iron deposition, or the pre-liver transplantation serum iron or ferritin levels. However, in the patients with myocardial iron deposition, there were trends toward higher pretransplant transferrin saturation (TSAT) and more units of red blood cells transfused (uRBC). The product of the TSAT multiplied by the uRBC was significantly greater in the patients with myocardial iron deposition [4700 (3100-9800) vs. 680 (400-2300), median (interquartile range), P=.003]. New reduced left ventricular ejection fraction (<50%) following liver transplantation occurred in four of five patients with myocardial iron deposition, compared with zero of eight patients without myocardial iron deposition (P=.007). In this series of patients without severe hepatic iron deposition, cardiac iron overload was associated with cardiac dysfunction following liver transplantation and was related to the product of the pre-liver transplant TSAT multiplied by the number of uRBC transfused during and following the surgery.