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Cardiac Cirrhosis and Congestive Hepatopathy

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Cardiac Cirrhosis and Congestive Hepatopathy


Author: Xiushui (Mike) Ren, MD; Chief Editor: Henry H Ooi, MB, MRCPI more...
Updated: Mar 2, 2012

Background
Cardiac cirrhosis (congestive hepatopathy) includes a spectrum of hepatic derangements that occur in the setting
of right-sided heart failure. Clinically, the signs and symptoms of congestive heart failure (CHF) dominate the
disorder. Unlike cirrhosis caused by chronic alcohol use or viral hepatitis, the effect of cardiac cirrhosis on overall
prognosis has not been clearly established. As a result, treatment is aimed at managing the underlying heart
failure.
Distinguishing cardiac cirrhosis from ischemic hepatitis is important. The latter condition may involve massive
hepatocellular necrosis caused by sudden cardiogenic shock or other hemodynamic collapse. Typically, sudden
and dramatic serum hepatic transaminase elevations lead to its discovery. Although cardiac cirrhosis and
ischemic hepatitis arise from distinct underlying cardiac lesions (right-sided heart failure in the former and leftsided failure in the latter), in clinical practice they may present together.
Despite its name, cardiac cirrhosis (which usually implies congestive hepatopathy that results in liver fibrosis)
rarely satisfies strict pathologic criteria for cirrhosis. The terms congestive hepatopathy and chronic passive liver
congestion are more accurate, but the name cardiac cirrhosis has become convention. For the remainder of this
chapter, the term cardiac cirrhosis will be used to mean congestive hepatopathy with or without liver fibrosis.

Cardiac cirrhosis. Congestive hepatopathy w ith large renal vein.

Cardiac cirrhosis. Congestive hepatopathy w ith large inferior vena cava.

Pathophysiology
Decompensated right ventricular or biventricular heart failure causes transmission of elevated right atrial pressure
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Cardiac Cirrhosis and Congestive Hepatopathy

to the liver via the inferior vena cava and hepatic veins. At a cellular level, venous congestion impedes efficient
drainage of sinusoidal blood flow into terminal hepatic venules. Sinusoidal stasis results in accumulation of
deoxygenated blood, parenchymal atrophy, necrosis, collagen deposition, and, ultimately, fibrosis.
A separate theory proposes that cardiac cirrhosis is not simply a response to chronically increased pressure and
sinusoidal stasis. Because intrahepatic vascular lesions are confined to areas of the liver with higher fibrotic
burden, cardiac cirrhosis may require a higher grade of vascular obstruction, such as intrahepatic thrombosis, for
its development. Thus, thrombosis of sinusoids and terminal hepatic venules propagates to medium-sized hepatic
veins and to portal vein branches, resulting in parenchymal extinction and fibrosis.

Epidemiology
Frequency
United States
Cardiac cirrhosis rarely occurs in the United States. Its true prevalence is difficult to estimate, since the disease
typically remains subclinical and undiagnosed. The incidence of cardiac cirrhosis at autopsy has decreased
significantly over the past several decades. This may be due to lower rates of uncorrected rheumatic heart disease
and constrictive pericardial disease.

Mortality/Morbidity
The effect of cardiac cirrhosis on mortality and morbidity rates is unknown. The severity of the patient's underlying
cardiac disease, which is typically advanced and chronic, is the major determinant of overall outcome.

Sex
Comparative sex data for cardiac cirrhosis do not exist. However, because CHF is more common in men than
women in the United States, the same is likely for cardiac cirrhosis.[1]

Age
No published data exist. However, the prevalence of cardiac cirrhosis in the United States, like that of CHF, almost
certainly increases with age.

Contributor Information and Disclosures


Author
Xiushui (Mike) Ren, MD Cardiovascular Physician, Department of Cardiology, Kaiser Medical Center;
Associate Director of Research, Cardiovascular Diseases Fellowship, California Pacific Medical Center
Xiushui (Mike) Ren, MD is a member of the following medical societies: Alpha Omega Alpha , American College
of Cardiology , and American Society of Echocardiography
Disclosure: Nothing to disclose.
Specialty Editor Board
Justin D Pearlman, MD, ME, PhD, FACC, MA Chief, Division of Cardiology, Director of Cardiology
Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory,
Director of Cardiology Quality Program KMC, Dartmouth-Hitchcock Medical Center, Dartmouth Medical School
Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American
College of Cardiology , American College of Physicians , American Federation for Medical Research ,
International Society for Magnetic Resonance in Medicine , and Radiological Society of North America
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

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Disclosure: Medscape Salary Employment


Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of California, Los Angeles, David
Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA
Biomedical Research Institute at Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC, FCCP is a member of the following medical societies: American College of
Cardiology , American College of Chest Physicians , American College of Physicians , American Heart
Association , and American Thoracic Society
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical
Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical
Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research
funds Clinical Trials + honoraria; LungRx Clinical Trials + honoraria; Bayer Grant/research funds Consulting;
Medtronic Consulting fee Consulting; Novartis Consulting fee Consulting
Amer Suleman, MD Private Practice
Amer Suleman, MD is a member of the following medical societies: American College of Physicians , American
Heart Association , American Institute of Stress , American Society of Hypertension , Federation of American
Societies for Experimental Biology , Royal Society of Medicine , and Society of Cardiac Angiography and
Interventions
Disclosure: Nothing to disclose.
Chief Editor
Henry H Ooi, MB, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville
Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine
Disclosure: Nothing to disclose.

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