THE LIVER IN CONGESTIVE HEART FAILURE
Jürg Reichen M.D.
Professor of Medicine, Dept. Clinical Pharmacology, University of Berne
    1. Incidence and pathophysiology:

      2. Abnormal liver enzymes and liver function in congestive, right-sided heart failure has long been recognized (13,17) and occurs quite frequently in acute and chronic failure (figure 1).

      This is thought to be due to direct centrizonal compression (18). It is less recognized that left-sided failure also leads to impairment of hepatic function due to a low-flow state (1-3,6,8). The mechanism is due to the fact that the liver gets a fixed amount of cardiac output (13); the decrease in flow is compensated for by an increase in oxygen extraction leading to anoxic necrosis in the centrizonal area. This is supported by a comparison of liver biopsies with and without centrizonal necrosis in patients with CHF; necrosis was only seen when also either marked venous congestion and/or hypoxemia existed (6). Of note is that even minor impairments of left ventricular function can lead to marked liver enzyme abnormalities (2,15); similarly, in known CHF, an episode of hypotension can be elicited in only 45 % (6). In chronic congestion, LFT's are abnormal dependent on the reduction in CO (10; figure 2).


       

    1. Manifestations: Range from laboratory abnormalities over a presentation undistinguishable from acute hepatitis to fulminant failure (3,14). The latter can lag behind the acute episode by 1 - 3 days (3); the latter authors found in their review of the literature a mortality of 69 % (11/16). Birgens et al. claim that hypotension of > 24 h is required for shock liver to develop (1); this is clearly not true - in up to 50 % of patients with hypoxic hepatitis no shock is observed (19). Hepatomegaly, often tender, in 95 - 99 % in right-sided failure, splenomegaly in 12 - 25 %; ascites 7 - 64 % (4). In CT mottled appearance of contrast, similar to Budd-Chiari (12).
    2. Laboratory: In right-sided heart failure hyperbilirubinemia rarely exceeds 50 mmoles/l and the transaminases are moderately elevated; occasionally isolated elevation of cholestatic enzymes. Vitamin-K refractory hypoprothrombinemia. In left-sided failure much more marked elevation of serum bilirubin (3) and of transaminases (3,5,9); typically, transaminase values tend to return very rapidly towards normal when the CHF is treated (5,14). According to the histologic lesion, ABT is reversibly decreased during the acute episode (7,16).
    3. Pathology: In right sided heart failure central necrosis, condensation of reticulin stroma. If of longer duration reverse lobulation and "cirrhose cardiaque" (4). In left sided failure disappearance of centrizonal hepatocytes with replacement by RBC's. No fibrosis (1). In both conditions, notable absence of inflammatory cells. In an autopsy review, midzonal necrosis was found to be typical of congestive failure, in particular when associated with episodes of hypotension occurring in 1.8 % of all autopsies in in 8 % of patients with centrizonal necrosis (3). In a review of 140 post-mortem specimens (figure 3), cardiac fibrosis was quite frequent but frank cirrhosis only observed once (11).



      Literature:

      1. Birgens H.S., Henriksen J., Matzen P., et al. 1978. The shock liver. Clinical and biochemical findings in patients with centrilobular necrosis following cardiogenic shock. Acta Med Scand 204:417-421.
      2. Cohen J.A. and Kaplan M.M. 1974. Left-sided heart failure presenting as hepatitis. Gastroenterology 74:583-587.
      3. De La Monte S.M., Arcidi J.M., Moore W.G., et al. 1984. Midzonal necrosis as a pattern of hepatocellular injury after shock. Gastroenterology 86:627-631.
      4. Dunn G.D., Hayes P., Breen K.J., et al. 1973. The liver in congestive heart failure: A review. Am J Med Sci 265:174-189.
      5. Field R.S. and Meyer G.W. 1978. Hepatic dysfunction in congestive heart failure simulating hepatitis. S Med J 71:221-222.
      6. Henrion J., Luwaert R., Colin L., et al. 1990. Hypoxic hepatitis. A prospective, clinical and hemodynamic study of 46 episodes. Gastroenterol Clin Biol 14:836-841.
      7. Hepner G.W., Vesell E.S. and Tantum K.R. 1978. Reduced drug elimination in congestive heart failure. Studies using aminopyrine as a model drug. Am J Med 65:371-376.
      8. Killip T. and Payne M.A. 1960. High transaminase activity in heart disease. Circulation 21:646-660.
      9. Kisloff B. and Schaffer G. 1976. Fulminant hepatic failure secondary to congestive heart failure. Am J Dig Dis 21:895-900.
      10. Kubo S.H., Walter B.A., John D.H.A., et al. 1987. Liver function abnormalities in chronic heart failure. Influence of systemic hemodynamics. Arch Int Med 147:1227-1230.
      11. Lefkowitch J.H. and Mendez L. 1986. Morphologic features of hepatic injury in cardiac disease and shock. J Hepatol 2:313-327.
      12. Moulton J.S., Miller B.L., Dodd G.D., et al. 1988. Passive hepatic congestion in heart failure: CT abnormalities. AJR 151:939-942.
      13. Myers J.D. and Hickam J.B. 1948. An estimation of hepatic blood flow and splanchnic oxygen consumption in heart failure. J Clin Invest 27:620-627.
      14. Nouel O., Henrion J., Bernuau J., et al. 1980. Fulminant hepatic failure due to transient circulatory failure in patients with chronic heart disease. Dig Dis Sci 25:49-52.
      15. Parisi P., DeVizia A., Macina G., et al. 1990. Acute liver disorders in left-sided heart failure. Ital J Gastroenterol 22:133-135.
      16. Pirotte J., El Allaf D., and Carlier J. 1983. Correlation between the demethylation rate of 14C-aminopyrine (breath-test) and haemodynamic parameters in congestive heart failure. Int J Clin Pharmacol Res 3:485-489.
      17. Richman S.M., Delman A.J., and Grob D. 1961. Alterations in indices of liver function in congestive heart failure with particular reference to serum enzymes. Am J Med 30:211-225.
      18. Shibayama Y. 1987. The role of hepatic venous congestion and endotoxaemia in the production of fulminant hepatic failure secondary to congestive heart failure. J Pathol 151:133-138.
      19. Henrion  J, Schapira M, Luwaert R et al. 2003. Hypoxic hepatitis - Clinical and hemodynamic study in 142 consecutive cases. Medicine 82: 392-406.


Written November 13th 1992
Put on WWW August 31st 2001, revised August 31st 2006