[1696] Histology of Liver Injury Secondary to Chronic Passive Congestion in Heart Failure

Christine Louie, Neeraja Kambham, Tami Daugherty, John Higgins. Stanford Hospital and Clinics, Stanford, CA

Background: Liver injury from chronic passive congestion from heart failure has been characterized based mostly on autopsy series. As a result, these series likely include agonal as well as autolytic changes in the liver parenchyma. Multiple reports of combined heart and liver transplant have been published from a surgical standpoint; however, no detailed descriptions of the histologic changes in livers seen in the context of combined transplant have been reported. We now describe the histologic findings observed in liver explants from patients receiving combined heart-liver transplants.
Design: We identified 6 cases of combined heart-liver transplants performed at our institution over a 10 year period from 2002-2012. For each case, the liver explant was examined by H&E, trichrome, reticulin, and elastic Van Gieson, and by immunohistochemistry for CD61. Clinical background and follow up was also obtained.
Results: The 6 patients identified all had heart failure related to either congenital heart disease or idiopathic dilated cardiomyopathy. All 6 livers showed changes that were felt secondary to cardiac dysfunction without other reasons for liver injury, including viral hepatitis. The changes included increased fibrosis, either in a bridging pattern, in a pericellular distribution, or both. Reticulin stains highlighted regenerative nodules in all cases. 3/6 cases showed patchy sinusoidal staining on CD61 stains, indicating platelet-fibrin deposition within sinusoids. 1/6 cases showed CD61 staining within blood vessels, and an additional case showed evidence of vessel obliteration on EVG with absence of CD61 staining, indicative of remote, organizing thrombosis. EVG stains also highlighted intimal thickening in 3 other cases, raising the possibility of resolved thrombosis. The liver injury also showed a patchy distribution; in all cases, the livers showed areas that appeared relatively uninvolved with no evidence of bridging fibrosis, sinusoidal dilation or architectural distortion.
Conclusions: In all cases examined, increased fibrosis and regenerative nodules were observed in all cases; however, the changes also showed a variable distribution, usually more abnormal in subcapsular areas. As every case showed uninvolved areas, none of the cases could be characterized as cirrhotic. Several cases showed areas of either remote or active thrombosis, suggesting a role for thrombosis in the development of fibrosis within cardiac livers. No significant hepatocellular necrosis was seen, suggesting that liver cell necrosis represents an agonal change that is not present in well compensated congestive heart failure.
Category: Liver

Wednesday, March 6, 2013 1:00 PM

Poster Session VI # 110, Wednesday Afternoon

 

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