bubble_chart Overview

Cardiac cirrhosis is caused by recurrent episodes of chronic congestive heart failure. Prolonged congestion and hypoxia lead to the proliferation of reticular fibrous tissue in the liver, primarily manifesting as stellate fibrosis in the central hepatic lobules. The fibrous tissue divides the hepatic lobules, forming irregular cell clusters known as pseudolobules.

bubble_chart Pathogenesis

Any disease that obstructs the return of inferior vena cava blood to the heart can lead to hepatic congestion, such as wind-dampness valvular heart disease, chronic constrictive pericarditis, hypertensive heart disease, ischemic heart disease, lung heart disease, congenital heart disease, etc.

Wind-dampness valvular heart disease ranks first among the causes of cardiogenic cirrhosis. Approximately 4–12% of wind-dampness valvular heart disease cases are complicated by cardiogenic cirrhosis, and 53.2% of cardiogenic cirrhosis cases are caused by wind-dampness valvular heart disease. When wind-dampness valvular heart disease leads to congestive heart failure, the pressure in the right atrium and right ventricle increases, impairing hepatic venous blood return and resulting in hepatic congestion and cirrhosis.

In chronic constrictive pericarditis, the thickened pericardium compresses the heart, severely limiting diastolic filling, leading to increased end-diastolic pressure in the right ventricle and elevated right atrial pressure. This obstructs hepatic venous blood flow, causing persistently high hepatic venous pressure, central hepatic sinus dilation, congestion, hemorrhage, and subsequent hypoxia and necrosis of hepatocytes. Central reticular fibrous tissue hyperplasia then leads to cardiogenic cirrhosis.

Hypertensive, coronary atherosclerotic, pulmonary, and congenital heart diseases, when complicated by right heart failure, can also obstruct hepatic venous blood flow, causing hepatic congestion and cirrhosis.

bubble_chart Pathological Changes

The liver is visibly enlarged, purplish in color, with blunt edges. After death or during autopsy, the liver often shrinks, and the cut surface may exhibit a "nutmeg" appearance, with alternating red and white areas—the red regions being hemorrhagic zones located around the portal tracts. Clinically, the severity of congestive heart failure does not absolutely correlate with the extent of hepatic lobular necrosis.

Congestive hepatic injury initially affects the central lobular area. Central lobular veins become congested and dilated, with the degree of sinusoidal dilation varying depending on their distance from the central lobular vein. Hepatocytes in the central lobule are compressed, deformed, and atrophic. The cytoplasm shows granular changes, with pyknosis, karyorrhexis, and cell necrosis, accompanied by brown pigmentation. The brown pigment is located centrally in the lobule, possibly due to cholestasis. The parenchyma adjacent to the central vein undergoes the most severe degeneration and necrosis. As congestion worsens, necrotic tissue extends toward the portal area, and in severe cases, only relatively normal liver tissue remains near the portal tracts. Over time, the reticular fibers around the central vein may collapse, revealing reticular fibrous tissue and fine fibrous bundles extending from one central vein to another. This fibrous bridging between adjacent central veins is characteristic of cardiac cirrhosis. Since most patients die from cardiovascular diseases, extensive regenerative nodules in the liver itself are rarely observed.

bubble_chart Clinical Manifestations

Patients with congestive heart failure accompanied by passive liver congestion primarily exhibit symptoms and signs caused by severe cardiac failure, while liver involvement is secondary. They may experience grade I right upper abdominal discomfort, with jaundice occurring in 10–20% of cases. Physical examination may reveal manifestations of congestive heart failure, including jugular vein distension and a positive hepatojugular reflux sign. Most patients present with hepatomegaly, while a few may exhibit significant enlargement, with 50% of patients having a liver extending more than 5 cm below the costal margin. In cases of secondary tricuspid regurgitation, an expansile hepatic pulsation may be palpable. As liver fibrosis develops, the liver may shrink back to normal size. Ascites is observed in 15% of patients, and splenomegaly in 25%.

bubble_chart Auxiliary Examination

1. Laboratory Tests

There is no absolute correlation between the degree of hepatic congestion and abnormal liver function. 80% of cases show bromsulphalein retention, while 25–75% exhibit elevated serum bilirubin. Serum alkaline phosphatase is mostly normal or only mildly elevated (grade I), whereas most other liver diseases are accompanied by an increase in serum alkaline phosphatase. This can help differentiate congestive hepatopathy from other liver diseases. In acute hepatic congestion, serum transaminases (AST, ALT) are significantly elevated, whereas in chronic congestion, the increase is only slight. Both acute and chronic hepatic congestion are associated with decreased albumin, increased globulin, and prolonged prothrombin time, which cannot be corrected by vitamin K but gradually normalizes as congestive heart failure improves. Additionally, with the improvement of congestive heart failure, other liver function indicators, particularly serum transaminases, return to normal quickly, while bromsulphalein retention tests take 1–2 weeks to normalize, and hypoprothrombinemia may take several weeks to resolve.

Generation and transformation indicators are not useful in distinguishing cirrhosis from non-cirrhotic conditions. Cardiac cirrhosis rarely shows abnormalities in these indicators, possibly because patients die from cardiovascular diseases before progressing to cardiac cirrhosis. The following conditions should raise suspicion of cardiac cirrhosis: ① severe rheumatic heart disease, especially mitral stenosis; ② chronic constrictive pericarditis; ③ recurrent or long-standing severe congestive heart failure; ④ severe hepatic congestion without hepatomegaly, but with ascites and splenomegaly; ⑤ tricuspid regurgitation without palpable expansile pulsation of the liver.

2. Liver Biopsy

This is a definitive diagnostic method. However, due to increased hepatic venous pressure in congestive heart failure, liver biopsy carries a higher risk of bleeding. Therefore, heart failure should be corrected and liver function normalized before biopsy. If an urgent biopsy is needed for diagnosis, it may still be performed if prothrombin time and platelet counts are within acceptable ranges.

bubble_chart Diagnosis

①Patients with severe congestive heart failure, accompanied by passive hepatic congestion, have an enlarged and tender liver. ②Serum bile acids and transaminases are grade I elevated, prothrombin time is prolonged, and serum alkaline phosphatase shows no significant changes. ③Liver function tests improve rapidly as congestive heart failure ameliorates. ④Liver biopsy can help confirm the diagnosis.

bubble_chart Treatment Measures

The primary goal is to correct or alleviate heart failure, using diuretics, cardiotonic drugs, and medications that reduce cardiac afterload. However, some symptoms in these patients are caused by the liver, such as refractory hypoglycemia and impaired consciousness, the latter also being related to reduced cardiac output.

Cardiogenic cirrhosis itself does not cause severe portal hypertension or esophageal variceal bleeding, but it can lead to splenomegaly and ascites. Palmar erythema, spider angiomas, and caput medusae are rare. Clinically, improvements in cardiac function—such as prosthetic valve replacement, relief of pericardial constriction in constrictive pericarditis, and correction of anatomical abnormalities in congenital heart disease—can gradually or even rapidly improve hepatocyte function.