We read with interest the articles by Arena et al.1 and Sagir et al.2 demonstrating that acute liver damage due to acute hepatitis induces a reversible increase in liver stiffness, which can mislead the diagnosis of liver cirrhosis. We report here another cause of false positive results of transient elastography, namely hepatic vascular congestion due to cardiac insufficiency.
A 58-year-old man was infected with hepatitis C virus genotype 3 in 1987 during two consecutive heart transplantations for severe ischemic cardiopathy followed by primary nonfunction of the graft. In 1999, a liver biopsy showed chronic hepatitis C with a METAVIR score of A1F1. Concerns of graft rejection precluded him from receiving antiviral treatment. In 2006, he developed progressive dyspnea related to severe coronary heart disease. This was later complicated by adiastolia, fibrous pericarditis, and inferior infarct with a 50% left ventricular ejection fraction. Brain natriuretic peptide increased to 800 IU/L. Ascites developed with high gamma glutamyl transpeptidase (GGT) (181 IU/L) and normal bilirubin, prothrombin time, and alanine aminotransferase (ALT) levels. Fibroscan (Echosens, France) showed high median liver elastometry at 44.3 kPa with an interquartile range of 10.2 and a 100% success rate compatible with liver cirrhosis. Decompensated HCV-related cirrhosis was suspected. However, upper gastrointestinal endoscopy was normal, while hepatic ultrasound did not show a dysmorphic liver or signs of portal hypertension but rather dilated hepatic veins and inferior vena cava compatible with cardiac hepatopathy. A transjugular liver biopsy (20 mm fragment with 11 portal spaces) confirmed major sinusoidal dilation, perisinusoidal fibrosis, and nodular hepatocyte regeneration compatible with cardiac hepatopathy and the absence of cirrhosis (Fig. 1). This prompted a third heart transplantation in February 2007.
The postoperative course was uneventful, and repeated myocardial ultrasound examinations and endomyocardial biopsies were normal. One year after the third heart transplantation, ALT was normal (17 IU/L), Fibroscan showed an elasticity of 3.8 kPa (interquartile range of 0.5 kPa, 100% success rate) and FibroTest a low value of 0.19, compatible with no or minimal fibrosis. Six months later, liver function tests slightly increased (ALT, 64 IU/L; GGT, 137 IU/L) with high HCV viremia. Another transjugular liver biopsy was performed (13 mm fragment with 13 portal spaces) and showed the disappearance of sinusoidal dilatation or perisinusoidal fibrosis. There was minimal intralobular necrosis without occasional portal fibrosis, and the histological diagnosis was chronic hepatitis C with a METAVIR score of A1F1 (Fig. 1B).
This case highlights the fact that vascular hepatic congestion can considerably increase hepatic elastometry, as measured by Fibroscan, to values that are unambiguously diagnostic for liver cirrhosis.3 This increase in elastometry is entirely reversible upon correction of cardiovascular dysfunction. Physicians should be aware of the possibility of false-positive diagnosis of cirrhosis or advanced fibrosis by transient elastography in patients with right-sided heart failure. Therefore, cardiac function should be systematically assessed in patients with high transient elastography values and no indication of liver fibrosis on other noninvasive fibrosis tests.