Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Cardiac Cirrhosis and Congestive Hepatopathy Workup

  • Author: Xiushui (Mike) Ren, MD; Chief Editor: Henry H Ooi, MD, MRCPI  more...
 
Updated: Dec 22, 2014
 

Laboratory Studies

Liver function tests

Evaluate severity of hepatic failure with liver function tests (LFTs), including hepatic transaminases, alkaline phosphatase, total bilirubin, and albumin.

The most common liver enzyme abnormality is an elevation of serum bilirubin. Patients with cardiac cirrhosis may exhibit modest elevations in aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, and total bilirubin, as well as mild decreases in albumin.

Abnormal values are more common in patients with mean right atrial pressures in excess of 10 mm Hg and cardiac indices less than 1.5 L/min/m2.

Abnormalities typically remain clinically silent and resolve with compensation of heart failure.

Extreme elevations of AST and ALT should alert the clinician to other causes of liver failure, including ischemic, toxic, and viral hepatitis.

Prothrombin time

A study from the 1960s showed prothrombin time (PT) to be abnormal in as many as 80% of patients with acute or chronic right-sided heart failure.

Other laboratory studies

Evaluate serial cardiac enzymes, CBC count, urinalysis, and routine serum electrolytes in a patient with cardiac cirrhosis in the setting of new-onset heart failure.

Search for evidence of reversible causes of CHF. For example, obtain levels of serum iron, total iron-binding capacity, and ferritin in an evaluation for hemochromatosis when cardiac cirrhosis presents with significant or persistent LFT abnormalities. Thyroid-stimulating hormone (TSH) levels are indicated in patients with unexplained cardiac cirrhosis and atrial fibrillation.

Next

Chest Radiography

Radiographic images may show cardiomegaly, pulmonary venous hypertension, interstitial or pulmonary edema, or pleural effusion. Pleural effusions typically are larger on the right.

Previous
Next

Echocardiography

Transthoracic echocardiogram with Doppler

An echocardiogram may diagnose the underlying cause of cardiac cirrhosis. Evaluation of biventricular size, mass, function, wall motion, and valves are indicated.

Because restrictive cardiomyopathy and pericardial constriction can lead to cardiac cirrhosis, specific attention should be paid to diastolic function parameters such as mitral inflow, pulmonary vein flow, mitral annular flow, and their responses to respiration.

Lack of inferior vena cava (IVC) respiratory variation (normally greater than or equal to 50% narrowing during inspiration) or IVC diameter greater than or equal to 2.3 cm suggest right-sided cardiac disease with increased right atrial filling pressures.

Subcostal Doppler view of hepatic veins demonstrating systolic flow reversal is highly specific for clinically significant tricuspid regurgitation.

Previous
Next

Radionuclide imaging

Radionuclide imaging with thallium or technetium is a noninvasive means to identify reversible cardiac ischemia in patients with cardiac cirrhosis in the setting of new or decompensated heart failure. Technetium-labeled agents and positron-emission tomography (PET) identify dilated cardiomyopathy and determine myocardial function.

Previous
Next

Abdominal Doppler Ultrasonography

Consider abdominal Doppler US in the setting of ascites, right upper quadrant abdominal pain, jaundice, and/or abnormal serum LFTs that are refractory to effective treatment of underlying heart failure. The test is performed to search for an alternative diagnosis, such as Budd-Chiari syndrome.

Previous
Next

Computed Tomography Scanning and Magnetic Resonance Imaging

CT scan and MRI help to diagnose restrictive and constrictive pericardial disease. These studies also may identify enlarged chamber size, ventricular hypertrophy, diffuse cardiomyopathy, valvular disease, and other structural abnormalities such as arrhythmogenic dysplasia of the right ventricle. Both can measure ejection fraction and effectively rule out cardiac cirrhosis. Body imaging may reveal evidence of cardiac cirrhosis, including hepatomegaly, hepatic congestion, IVC enlargement, and splenomegaly (see following images).

Cardiac cirrhosis. Congestive hepatopathy with lar Cardiac cirrhosis. Congestive hepatopathy with large renal vein.
Cardiac cirrhosis. Congestive hepatopathy with lar Cardiac cirrhosis. Congestive hepatopathy with large inferior vena cava.
Previous
Next

Electrocardiography

Evidence of prior myocardial infarction, ventricular hypertrophy, and right atrial enlargement is common.

Right ventricular hypertrophy, right axis deviation, and right bundle-branch block may suggest chronic right ventricular pressure overload.

Previous
Next

Paracentesis

Diagnostic paracentesis may distinguish between cardiac and other etiologies of ascites. The information is useful especially in patients with chronic alcoholism and uncharacterized cardiac disease. Evaluate fluid for cell count and differential, albumin, total protein, and cytology.

Typically, cardiac ascites will reveal a high serum-ascites albumin gradient (SAAG) greater than 1.1 g/dL and a high ascitic fluid total protein greater than 2.5 g/dL. Patients with cirrhotic ascites also have a high SAAG value, but ascitic fluid total protein will be greater than 2.5 g/dL only 10% of the time.[6] See the Ascites Albumin Gradient calculator.

Employ therapeutic paracentesis for ascites refractory to diuretic treatment. Because hepatic albumin synthetic function usually is preserved in cardiac cirrhosis, parenteral albumin supplementation after paracentesis is not indicated.

Previous
Next

Cardiac Catheterization and Coronary Angiography

The procedure may be indicated in patients with cardiac cirrhosis and heart failure in the context of known or suspected coronary artery disease. The study is employed primarily to evaluate coronary arterial anatomy and the need for revascularization.

Perform right heart catheterization to diagnose pulmonary hypertension in the setting of suggestive physical examination or echocardiographic findings.

In less than 1% of patients with chronic liver failure, pulmonary hypertension occurs in the absence of underlying pulmonary or cardiac disease. This entity, known as portopulmonary hypertension, may progress to right ventricular failure and present a diagnostic challenge to determine whether liver failure or heart disease is the primary lesion.

Previous
Next

Biopsy

Needle liver biopsy

The procedure is not indicated routinely. Needle biopsy is indicated in heart transplant candidates with ascites to rule out cirrhosis.

Endomyocardial biopsy

The procedure may be indicated in patients with cardiac cirrhosis with deteriorating clinical condition and a strong clinical suspicion for myocarditis. It also may be indicated in the presence of a systemic disease with possible cardiac involvement, such as hemochromatosis or sarcoid.

Previous
Next

Histologic Findings

Cardiac cirrhosis is associated with characteristic histologic changes. The presence of centrilobular parenchymal atrophy, sinusoidal and terminal hepatic venular distention, and perisinusoidal collagen deposition establishes chronic passive hepatic congestion (CPC).

In more severe cases, centrilobular fibrosis develops and eventually may include diffuse fibrous septa[7] and regenerative nodules characteristic of true cirrhosis.

Histologic findings are bland, with an absence of inflammatory cells.

Exposure of the liver to venous hypertension alone has not been demonstrated to cause centrilobular necrosis (CLN); in practice, however, histologic features of both CPC and CLN frequently occur together. CPC and CLN form a morphological continuum reflecting degrees of preexisting hepatic congestion and acute liver hypoperfusion. The synergistic combination of CPC and CLN is known as centrilobular hemorrhagic necrosis, referred to more commonly as nutmeg liver.[8]

The liver's mottled gross appearance results from the contrast of red-brown centrilobular regions suffused with blood against viable, if somewhat fatty, periportal tissue.

Previous
 
 
Contributor Information and Disclosures
Author

Xiushui (Mike) Ren, MD Cardiologist, The Permanente Medical Group; 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, American Society of Echocardiography

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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 Thoracic Society, American College of Physicians, American Heart Association

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Actelion, Bayer, Gilead, Lung Biotechnology, United Therapeutics<br/>Received research grant from: Actelion, Bayer, Gilead, Ikaria, Lung Biotechnology, Pfizer, Reata, United Therapeutics<br/>Received income in an amount equal to or greater than $250 from: Actelion, Bayer, Gilead, Lung Biotechnology, Medtronic, Reata, United Therapeutics.

Chief Editor

Henry H Ooi, MD, 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.

Additional Contributors

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, Chair of Institutional Review Board, University of California, Los Angeles, David Geffen School of Medicine

Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology, International Society for Magnetic Resonance in Medicine, American College of Physicians, American Federation for Medical Research, Radiological Society of North America

Disclosure: Nothing to disclose.

References
  1. Moller S, Bernardi M. Interactions of the heart and the liver. Eur Heart J. 2013 Sep. 34(36):2804-11. [Medline].

  2. Fouad YM, Yehia R. Hepato-cardiac disorders. World J Hepatol. 2014 Jan 27. 6(1):41-54. [Medline]. [Full Text].

  3. Burns RB, McCarthy EP, Moskowitz MA. Outcomes for older men and women with congestive heart failure. J Am Geriatr Soc. 1997 Mar. 45(3):276-80. [Medline].

  4. Shapira, Y, Porter, A, Wurzel, M. Evaluation of tricuspid regurgitation severity: echocardiographic and clinical correlation. J Am Soc Echocardiogr. 1998 Jun. 11(6):652-9. [Medline].

  5. Yoo BW, Choi JY, Eun LY, et al. Congestive hepatopathy after Fontan operation and related factors assessed by transient elastography. J Thorac Cardiovasc Surg. 2014 Oct. 148(4):1498-505. [Medline].

  6. Runyon BA. Cardiac ascites: a characterization. J Clin Gastroenterol. 1988 Aug. 10(4):410-2. [Medline].

  7. Wanless IR, Liu JJ, Butany J. Role of thrombosis in the pathogenesis of congestive hepatic fibrosis (cardiac cirrhosis). Hepatology. 1995 May. 21(5):1232-7. [Medline].

  8. Arcidi JM, Moore GW, Hutchins GM. Hepatic morphology in cardiac dysfunction: a clinicopathologic study of 1000 subjects at autopsy. Am J Pathol. 1981 Aug. 104(2):159-66. [Medline].

  9. Fava M, Meneses L, Loyola S, Castro P, Barahona F. TIPSS Procedure in the Treatment of a Single Patient After Recent Heart Transplantation Because of Refractory Ascites Due to Cardiac Cirrhosis. Cardiovasc Intervent Radiol. December 2007. [Medline]. [Full Text].

  10. Dichtl W, Vogel W, Dunst KM, Grander W, Alber HF, Frick M, et al. Cardiac hepatopathy before and after heart transplantation. Transpl Int. 2005 Jun. 18(6):697-702. [Medline].

 
Previous
Next
 
Cardiac cirrhosis. Congestive hepatopathy with large renal vein.
Cardiac cirrhosis. Congestive hepatopathy with large inferior vena cava.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.