AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

Section 2 of 11  

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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 is unknown. Because of this, treatment is aimed at managing the patient's underlying heart failure.

Distinguish cardiac cirrhosis from ischemic hepatitis. 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 left-sided failure in the latter), in clinical practice they may present together.

Despite its name, cardiac cirrhosis 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.

Pathophysiology

Decompensated right ventricular or biventricular heart failure causes transmission of elevated central venous pressures directly 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. That intrahepatic vascular lesions are confined to areas of the liver with higher fibrotic burden suggests that cardiac cirrhosis requires a higher grade of vascular obstruction, such as intrahepatic thrombosis, for its development. The theory proposes that thrombosis of sinusoids and terminal hepatic venules propagates to medium-sized hepatic veins and to portal vein branches, resulting in parenchymal extinction and fibrosis.

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.

Age

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

CLINICAL

Section 3 of 11  

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History

Symptoms of CHF almost always mask gastrointestinal symptoms. Symptoms typically progress insidiously but may present suddenly and dramatically in cases of constrictive pericarditis or acute right ventricular decompensation. Patients may present with asymptomatic liver enzyme abnormalities, jaundice, and right upper quadrant discomfort. Case reports of fulminant hepatic failure have also been reported.

• In addition to CHF, a patient's past medical history is likely to include one or more of the following:
• • Coronary artery disease
  • Myocardial infarction
  • Hypertension
  • Dilated cardiomyopathy
  • Valvular heart disease
  • Chronic alcohol abuse
  • Chronic obstructive pulmonary disease (COPD)
  • Cor pulmonale
  • Pulmonary hypertension
  • Constrictive pericarditis
  • Rheumatic heart disease
• Symptoms may be divided into those that accompany right ventricular heart failure and the additional findings of biventricular failure.
• • Symptoms associated with isolated right-sided heart failure
    • Dependent edema and weight gain
    • Increased abdominal girth
    • Right upper quadrant abdominal pain
    • Nocturia
    • Progressive fatigue
    • Anorexia, nausea, and vomiting
  • Symptoms associated with biventricular heart failure
    • Progressive dyspnea
    • Orthopnea
    • Paroxysmal nocturnal dyspnea
    • Wheezing and/or cough (ie, cardiac asthma)
    • Anxiety: Multifactorial causes include dyspnea, palpitations, and increased sympathetic tone.

Physical

Signs of heart failure dominate the physical examination findings.

• Edema typically occurs in the lower extremities and dependent regions, which may progress to anasarca in cases of advanced and untreated heart failure. Chronic edema may be associated with lower extremity pigmentation, induration, and cellulitis.
• Jugular venous pressure is elevated.
• • Further distention of neck veins may be elicited with application of pressure over the right upper quadrant for as long as 1 minute (ie, hepatojugular reflux).
  • Paradoxical rise in jugular venous pressure during inspiration (ie, Kussmaul sign) may indicate constrictive pericarditis, right ventricular heart failure, tricuspid stenosis, or cor pulmonale.
  • Right atrial pressure recordings reveal large a waves, indicating elevated right atrial pressure that may appear as presystolic liver pulsations.
  • Prominent v waves with rapid y descent indicate tricuspid regurgitation. Progression to a systolic, or c-v, wave occurs in severe tricuspid insufficiency and may appear as systolic liver pulsations.
• Rales on lung examination indicate biventricular CHF. Decreased basilar breath sounds from pleural effusion also are common.
• Cardiac examination may reveal abnormalities related to right ventricular failure, tricuspid regurgitation, or both.
• • Abnormal systolic sternal or left parasternal lift signifies both pulmonary and right ventricular hypertension.
  • Right ventricular third and fourth heart sounds commonly are appreciated at the lower left sternal border of the sternum or over the xiphoid. Right ventricular S3 suggests right ventricular failure. Right ventricular S4 results from right atrial contraction into a noncompliant right ventricle. Inspiration increases the intensity of both extra heart sounds.
  • The holosystolic, high-pitched, blowing murmur of tricuspid insufficiency often accompanies severe right ventricular dilation and failure. The murmur is best heard at the lower left sternal border. But in cases of severe right ventricular enlargement, the murmur may be displaced as far laterally as the left midclavicular line. The murmur intensifies with inspiration and decreases with expiration.
  • Signs of pulmonary hypertension include a closely split S2 with a loud pulmonic component. The Graham Steell murmur of pulmonary hypertensive pulmonic regurgitation is a high-pitched, blowing diastolic murmur beginning with a loud P2 and continuing through most of diastole.
• Hepatomegaly is common, usually presenting as a firm, hard liver.
• • Elevated hydrostatic pressure within the hepatic veins and the peritoneal venous drainage system causes cardiac ascites. Protein-losing enteropathy with subsequent reduction of plasma oncotic pressure also may exacerbate ascites.
  • Splenomegaly may be found.
  • Fewer than 10% of patients exhibit jaundice.
  • Hepatic encephalopathy is rare.
• Anorexia, weight loss, and malnutrition (ie, cardiac cachexia) indicate advanced underlying heart disease.

Causes

Causes of cardiac cirrhosis mirror the many etiologies of right-sided CHF. Although inferior vena caval thrombosis and Budd-Chiari syndrome exhibit similar pathophysiology, they are categorized separately and are not included as causes of cardiac cirrhosis.

The most frequent causes of cardiac cirrhosis are the following:

• Ischemic heart disease (31%)
• Cardiomyopathy (23%)
• Valvular heart disease (23%)
• Primary lung disease (15%)
• Pericardial disease (8%)

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Congestive heart failure, biventricular
Congestive heart failure, right ventricular
Hepatic veno-occlusive disease
Hepatitis, ischemic

WORKUP

Section 5 of 11  

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Lab Studies

• 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 (PT): One study from the 1960s showed prothrombin time to be abnormal in as many as 80% of patients with acute or chronic right-sided heart failure.
• 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.
• • Serum iron, total iron-binding capacity, and ferritin: An evaluation for hemochromatosis is indicated when cardiac cirrhosis presents with significant or persistent LFT abnormalities.
  • Thyroid-stimulating hormone (TSH): TSH level is indicated in patients with unexplained cardiac cirrhosis and atrial fibrillation.

Imaging Studies

• Chest radiography: Images may show cardiomegaly, pulmonary venous hypertension, interstitial or pulmonary edema, or pleural effusion. Pleural effusions typically are larger on the right.
• Transthoracic Doppler 2-dimensional echocardiogram: An echocardiogram may diagnose the underlying cardiac lesion responsible for cardiac cirrhosis. Evaluation of left and right ventricular function and wall thickness, chamber sizes, wall motion, valvular disease, and right ventricular systolic hypertension is indicated.
• • 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.
• 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.
• Abdominal Doppler ultrasonography (US): 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.
• CT scan and MRI: CT scan and MRI diagnose restrictive and constrictive pericardial disease. These studies also may identify enlarged chamber size, ventricular hypertrophy, diffuse cardiomyopathy, valvular disease, and other structural abnormalities. 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 Images 1-2).

Other Tests

• 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.
• Digital pulse oximetry

Procedures

• 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.
  • 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.
• Cardiac catheterization/coronary angiography: The procedure may be indicated in patients with cardiac cirrhosis and heart failure in the context of known coronary artery disease, anginal symptoms, wall motion abnormalities on ECG, or multiple cardiac risk factors. 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.
• 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.

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 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.
• 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.

TREATMENT

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Medical Care

No prospective studies have been performed to evaluate the medical treatment of cardiac cirrhosis. Because no data suggest that the presence of cardiac cirrhosis worsens mortality or morbidity rates, direct treatment at the underlying source of elevated right-sided heart pressure and hepatic venous congestion.

• Initiate treatment in an inpatient setting, both to rule out ischemic heart disease and to administer IV diuretics.
• In most cases, diuresis is the cornerstone of initial medical therapy.

Surgical Care

Definitive treatment of cardiac cirrhosis sometimes requires surgical intervention, particularly when the underlying structural or anatomic lesion remains symptomatic despite maximal medical therapy.

• Examples of surgical intervention include the following:
• • Coronary artery bypass surgery or percutaneous transluminal coronary angioplasty for ischemic cardiomyopathy
  • Tricuspid valve repair or replacement for tricuspid regurgitation or tricuspid stenosis
  • Pericardiectomy (cardiac decortication) for constrictive pericarditis
  • Peritoneovenous shunt not indicated to treat cardiac ascites
• Transjugular intrahepatic portosystemic shunt (TIPSS) is contraindicated owing to the risk of acute right-sided decompensation from increased venous return.

Consultations

• Cardiology
• Gastroenterology
• Diet and/or nutrition

Diet

Sodium restriction is a fundamental component of long-term management.

• The sodium intake goal is less than 2 g/d.

Activity

A sensible exercise program is appropriate for most patients with cardiac cirrhosis after medical control of their underlying heart failure.

MEDICATION

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With few exceptions (eg, acute right ventricular myocardial infarction), diuresis is the cornerstone of initial management of cardiac cirrhosis. As cardiac cirrhosis is a direct complication of elevated central venous pressures, effective diuresis should improve hepatic derangements. Lack of improvement should prompt a search for primary hepatic disease.

Beyond diuretics, medical therapy should be directed at treating underlying heart failure and correcting the source of elevated right-sided heart pressures.

Drug Category: Diuretics

Initial treatment of cardiac cirrhosis usually requires a loop diuretic (eg, furosemide). Spironolactone may provide additional diuresis through its aldosterone antagonism effects.

Drug Name	Spironolactone (Aldactone)
Description	For management of edema resulting from excessive aldosterone levels secondary to hepatic cirrhosis or CHF. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.
Adult Dose	25-200 mg/d PO in 1-2 divided doses
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; anuria; renal failure; hyperkalemia
Interactions	May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity; ACE inhibitors or NSAIDs may result in severe hyperkalemia; may increase serum digoxin levels
Pregnancy	D - Unsafe in pregnancy
Precautions	Perform frequent tests of serum potassium and renal function during first few months of therapy and periodically thereafter; avoid concomitant potassium supplementation

FOLLOW-UP

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Further Inpatient Care

• With few exceptions, patients presenting with cardiac cirrhosis and acute heart failure symptoms require hospital admission. This is particularly true in the initial presentation of heart failure.
• Admission also is indicated when chronic symptoms become refractory to outpatient therapy and large doses of oral diuretics do not provide adequate diuresis.
• Consider initial admission to a telemetry unit for continuous ECG monitoring.

Further Outpatient Care

• Instruct patients to maintain a diary of their daily weights. Specific instructions may be issued to increase the patient's oral diuretic dose, as well as to return for immediate medical evaluation when certain weight increases are exceeded (eg, 2 lb/d or 5 lb/wk).
• Schedule periodic follow-up.
• • Monitor symptoms, preferably using well-defined activities (eg, walking 100 ft on ground level, climbing 1-2 flights of stairs).
  • Follow serum levels of potassium, BUN, and creatinine.
  • Follow serum levels of AST, ALT, alkaline phosphatase, and total bilirubin. All should normalize with attainment of heart failure compensation.
  • Failure of levels to resolve despite heart failure resolution should prompt evaluation of noncardiac sources of liver disease.

Transfer

• Consider initial transfer to a telemetry ward for continuous ECG monitoring with new presentations of cardiac cirrhosis.
• Transfer to a tertiary care facility may be warranted for surgical treatment of the following:
• • Atherosclerotic coronary artery disease - Either with percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass surgery
  • Severe valvular disease
  • Constrictive pericarditis

Deterrence/Prevention

• The patient may prevent hospitalization for heart failure by enrolling in a heart failure clinic or agreeing to frequent brief physician visits for any of the following:
• • Reinforcing recognition of early heart failure symptoms
  • Close following of daily weight log
  • Encouraging adherence to a low-sodium diet
  • Reviewing medical compliance
  • Drug interactions

Complications

• Acute renal failure secondary to overdiuresis

Prognosis

• The independent effect of cardiac cirrhosis on morbidity or mortality rate is unknown.
• Prognosis is based on the patient's underlying heart failure condition.

Patient Education

• Additional patient information may be found at Heart Failure Online and Heart Information Network.
• For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education article Congestive Heart Failure.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failure to diagnose a correctable underlying cause of cardiac cirrhosis is a potential pitfall. For example, patients with alcoholism and cardiac disease who present with ascites may be misdiagnosed by attributing liver derangements to alcoholic cirrhosis.
• Failure to search for concomitant hepatobiliary disease in patients with either significantly or persistently elevated hepatic transaminases, alkaline phosphatase, or total bilirubin levels is a potential pitfall. For example, collecting a detailed social history may lead to the diagnosis of acute hepatitis B infection and prevent progression to end-stage liver failure.
• Performing unnecessary liver biopsy is a potential pitfall.
• Transjugular intrahepatic portosystemic shunt (TIPSS) is contraindicated in cardiac cirrhosis. It may precipitate acute right heart failure from an acute increase in pulmonary arterial pressure.
• Failure to adjust hepatically cleared medications is a potential pitfall.

MULTIMEDIA

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Media file 1:  Cardiac cirrhosis. Congestive hepatopathy with large renal vein.
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Media type:  CT

Media file 2:  Cardiac cirrhosis. Congestive hepatopathy with large inferior vena cava.
	View Full Size Image
Media type:  CT

REFERENCES

Section 11 of 11

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• Cotran RS. Robbins Pathologic Basis of Disease. 6th ed. Philadelphia: WB Saunders Co;1999:117,883.
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• Dunn GD, Hayes P, Breen KJ. The liver in congestive heart failure: a review. Am J Med Sci. 1973;265:174.
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• Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol. Aug 15 1990;66(4):493-6. [Medline].
• Kubo SH, Walter BA, John DH. Liver function abnormalities in chronic heart failure. Influence of systemic hemodynamics. Arch Intern Med. Jul 1987;147(7):1227-30. [Medline].
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• Naschitz JE, Slobodin G, Lewis RJ. Heart diseases affecting the liver and liver diseases affecting the heart. Am Heart J. Jul 2000;140(1):111-20. [Medline].
• Richman SM, Delman AJ, Grob D. Alterations in indices of liver function in congestive heart failure with particular reference to serum enzymes. Am J Med. Feb 1961;30:211-225.
• Runyon BA. Cardiac ascites: a characterization. J Clin Gastroenterol. Aug 1988;10(4):410-2. [Medline].
• Schlant RC, Hurst JW. Examination of the Precordium: Inspection and Palpation. American Heart Association;1990:15-16.
• Sekiyama T, Nagano T, Aramaki T. [Congestive (cardiac) cirrhosis]. Nippon Rinsho. Jan 1994;52(1):229-33. [Medline].
• Shapira, Y, Porter, A, Wurzel, M. Evaluation of tricuspid regurgitation severity: echocardiographic and clinical correlation. J Am Soc Echocardiogr. Jun 1998;11(6):652-9. [Medline].
• Shaver JA, Leonard JJ, Leon DF. Auscultation of the Heart. American Heart Association;1990:28-49.
• Wanless IR, Liu JJ, Butany J. Role of thrombosis in the pathogenesis of congestive hepatic fibrosis (cardiac cirrhosis). Hepatology. May 1995;21(5):1232-7. [Medline].
• Williams JF. Guidelines for the evaluation and management of heart failure. Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Evaluation and Management of Heart Failure). Circulation. Nov 1 1995;92(9):2764-84. [Medline].

Article Last Updated: Aug 28, 2006