Cardiology > Cardiac Cirrhosis (Congestive Hepatopathy) 

Background

Cardiac cirrhosis, also known as congestive hepatopathy, is liver injury and fibrosis resulting from chronic passive congestion due to right-sided heart failure. The hepatic venous outflow obstruction causes elevated central venous pressure, leading to sinusoidal dilation, centrilobular necrosis, and eventually bridging fibrosis and cirrhosis. Unlike classic cirrhosis, synthetic liver function is often preserved until late stages.

II) Classification/Types

By Onset: 

• • Acute Congestive Hepatopathy: Rapid passive congestion, usually in acute decompensated heart failure or cardiac tamponade. 

• • Chronic Congestive Hepatopathy: Long-standing right heart failure leading to fibrosis. 

• • Cardiac Cirrhosis: Advanced chronic hepatic fibrosis due to longstanding hepatic congestion. 

By Etiology of Cardiac Disease: 

• • Right heart failure (e.g., pulmonary hypertension, tricuspid regurgitation) 

• • Constrictive pericarditis 

• • Restrictive cardiomyopathy 

• • Severe left-sided heart failure with biventricular involvement 

III) Pathophysiology 

Increased central venous pressure impedes hepatic venous outflow. This causes centrilobular (zone 3) sinusoidal congestion and hepatocyte atrophy. Over time, repeated injury leads to pericentral fibrosis, then bridging fibrosis and nodular regenerative changes consistent with cirrhosis. Hepatic arterial flow may also be compromised, leading to superimposed ischemic injury. 

IV) Epidemiology

• • Sex: No strong gender predilection; determined by underlying heart disease. 

• • Age: More common in older adults with chronic cardiac conditions. 

• • Geography: Global prevalence mirrors the burden of chronic heart failure. 

• • Comorbidities: Strongly associated with pulmonary hypertension, tricuspid regurgitation, cor pulmonale, constrictive pericarditis, and congenital heart disease. 

Etiology

I) Causes

• • Right-sided heart failure (e.g., cor pulmonale, tricuspid valve disease) 

• • Constrictive pericarditis 

• • Restrictive cardiomyopathy (e.g., amyloidosis) 

• • Severe pulmonary hypertension 

• • Chronic left heart failure with elevated right-sided pressures 

• • Congenital heart disease (e.g., Eisenmenger syndrome) 

II) Risk Factors

• • Chronic heart failure (especially right-sided) 

• • Pulmonary hypertension 

• • History of cardiac surgery or pericardial disease 

• • Tricuspid regurgitation 

• • Atrial fibrillation (due to chronic congestion) 

• • Advanced age 

Clinical Presentation

I) History (Symptoms)

• • Fatigue and malaise 

• • Abdominal fullness or discomfort 

• • Right upper quadrant pain (due to hepatic capsule distension) 

• • Peripheral edema and ascites 

• • Dyspnea (due to underlying heart failure) 

• • Early satiety and weight gain (due to fluid overload) 

II) Physical Exam (Signs)

Vital Signs: 

• • Tachycardia (in decompensated states) 

• • Hypotension (in severe cardiac dysfunction) 

Cardiac Exam: 

• • Elevated jugular venous pressure (JVP) 

• • Right ventricular heave 

• • Holosystolic murmur (tricuspid regurgitation) 

Abdominal Exam: 

• • Hepatomegaly (tender, pulsatile liver in early disease) 

• • Ascites 

• • Splenomegaly (less common than in portal hypertension from cirrhosis) 

• • Positive hepatojugular reflux 

Peripheral: 

• • Pitting edema 

• • Cyanosis (in advanced heart failure) 

Differential Diagnosis (DDx)

• • Alcoholic liver disease 

• • Viral hepatitis (HBV, HCV) 

• • Non-alcoholic steatohepatitis (NASH) 

• • Hemochromatosis 

• • Budd-Chiari syndrome 

• • Primary biliary cholangitis 

• • Autoimmune hepatitis 

• • Right heart failure without liver involvement 

Diagnostic Tests

Initial Tests: 

Liver Function Tests (LFTs): 

• • Mild elevations in AST, ALT (typically <2x ULN) 

• • Disproportionate elevation in alkaline phosphatase and bilirubin 

• • Elevated INR and low albumin in advanced cirrhosis 

Serum Markers: 

• • Elevated BNP/NT-proBNP (suggests cardiac source) 

• • Hypoalbuminemia (in chronic disease) 

Imaging: 

Ultrasound: 

• • Enlarged, hypoechoic liver 

• • Dilated hepatic veins and IVC 

• • Ascites 

Doppler Ultrasound: 

• • Decreased hepatic venous flow or reversed waveform 

• • Pulsatile portal vein (sign of cardiac backpressure) 

CT/MRI: 

• • “Nutmeg liver” appearance 

• • Signs of fibrosis or cirrhosis 

• • Cardiac chamber enlargement 

Echocardiography: 

• • Essential to assess underlying cardiac function (e.g., tricuspid regurgitation, RV dysfunction) 

Liver Biopsy: 

• • Confirms centrilobular fibrosis, sinusoidal congestion 

• • Reserved for unclear diagnosis 

Treatment

I) Medical Management:

Optimize Cardiac Function: 

• • Diuretics (loop ± thiazide) to manage volume overload 

• • Afterload reduction (ACE inhibitors, ARBs) 

• • Aldosterone antagonists in heart failure 

• • Digoxin or beta-blockers in atrial fibrillation 

Manage Complications of Cirrhosis: 

• • Sodium restriction and diuretics for ascites 

• • Paracentesis for tense ascites 

• • Avoid hepatotoxic medications 

• • Monitor for coagulopathy and hepatic encephalopathy 

II) Surgical/Advanced Therapies:

• • Valve repair or replacement for underlying tricuspid or pulmonary valve disease 

• • Pericardiectomy for constrictive pericarditis 

• • Heart transplantation for end-stage cardiac disease 

• • Liver transplantation generally not indicated unless dual pathology 

Patient Education, Screening, Vaccines

• • Importance of strict adherence to heart failure medications 

• • Daily weight monitoring for fluid retention 

• • Avoid high-sodium diet and excessive fluid intake 

• • Abstain from alcohol and hepatotoxic drugs 

• • Monitor for symptoms of hepatic decompensation (jaundice, encephalopathy) 

Vaccinations: 

• • Hepatitis A and B (if not immune) 

• • Influenza annually 

• • Pneumococcal vaccine 

• • COVID-19 vaccine 

Consults

• • Cardiology: All patients for heart failure optimization and valve evaluation 

• • Hepatology: For advanced fibrosis, unclear diagnosis, or liver-related complications 

• • Nutrition: For dietary counseling (e.g., sodium restriction) 

• • Palliative Care: In patients with refractory symptoms or advanced disease 

• • Primary Care/Internal Medicine: Coordination of chronic disease management 

Follow-Up

• • LFTs and synthetic markers every 3–6 months in chronic disease 

• • Echocardiogram annually or with symptom progression 

• • Ultrasound/Doppler every 6–12 months to monitor congestion or ascites 

• • Monitor for signs of hepatic decompensation: ascites, encephalopathy, variceal bleeding 

• • Adjust diuretic and heart failure therapy as needed 

• • Educate on early warning signs and need for urgent care