All patients also had a transthoracic echocardiogram (TTE) performed prior to MRI. Logistic regression was used to identify predictors of waitlist and post LT outcomes. Results: Median age of the eligible cohort (n=129) was 56 years (IQR 50-61). 71% were male and 43% were Caucasian. Hepatitis C was the most common etiology of liver disease (50%). Median MELD at time of T2* was 24 and 67% of patients were Child-Pugh class C (CP-C). Seventy-six patients had HFE gene mutation analysis tested, 7 (9%) of whom had high-risk mutations (C282Y/C282Y or C282Y/H63D). Median ferritin was 1477 μg/L (IQR 11732270) and median iron and transferrin saturation were 137.5 μg/dL and 86%, respectively. Median left

ventricular ejection fraction (LVEF) on TTE was 68% (IQR 64-73) and diastolic Decitabine dysfunction was found in 28%. Median T2* was 29 ms and 28 patients (22%) had a value <20ms. On multivariate analysis, CP-C (HR 4.9, 95% CI 1.4-16.4, p=0.01), ferritin>2000 μ/L (HR 2.8, 95% CI 1.1-7.2, p=0.03), and LVEF on TTE (HR 1.5 (per 5% drop),

95% CI 1.1-1.9, p=0.01) were associated with having a T2* <20ms. Overall, 62 this website patients (48%) received LT, 38% were delisted (7 due to T2*<10ms), and 12% are still waiting. Thirteen patients with a T2* 11-20ms underwent LT and 4 of these (31%) had immediate post LT HF whereas only 1 of 49 patients (2.0%) with a T2*>20ms experienced post LT HF (p=0.01). Two of the 5 patients with post LT HF died. In addition to T2* <20ms, lower LVEF on echocardiogram was also associated with post LT HF (p=0.04). Conclusion: In LT candidates at risk for iron overload, severity of liver disease, lower TTE LVEF and ferritin levels>2000 ug/L were associated with T2* <20ms, which in turn was associated with post LT HF. As over 30% of patients with T2* values between 10-20ms developed post LT HF, early involvement of HF specialists is prudent for both pre-LT patient selection decisions and for close management mafosfamide in the

peri-transplant period. Disclosures: The following people have nothing to disclose: Moises Nevah Rubin, Monika Sarkar, Karen Ordovas, Oren K. Fix, Neil Mehta Background: Hepatic injury induced by carbon tetrachloride (CCl4) is a well-known chemical-induced hepatocyte injury. However, the role of Kupffer cells in this model is still in controversy. We previously reported that F4/80+ Kupffer cells are subclassified into two subsets, the CD68+ population with phagocytic, ROS producing and bactericidal capacities, and CD11b+ population with cytokine-producing and antitumor capacities in mice and humans. Based on this theory, the present study investigated the immunological role of Kupffer cells/ macrophages in CCl4-induced hepatitis. Methods: C57BL6 mice were administered with CCl4 intra-peritoneally and examined dynamics of Kupffer cell populations, intracellular TNF and surface Fas-ligand (FasL) expression by flow cytometry.