Congestive Hepatopathy Secondary to Right Ventricular Hypertrophy Related to Monocrotaline-Induced Pulmonary Arterial Hypertension

Heart dysfunction and liver disease often coexist. Among the types of cardiohepatic syndrome, Type 2 is characterized by the chronic impairment of cardiac function, leading to chronic liver injury, referred to as congestive hepatopathy (CH). In this study, we aimed to establish a rat model of CH secondary to right ventricular hypertrophy (RVH) related to monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH). Fifty male Wistar rats were divided into four groups and randomly assigned to control and experimental groups. Three experimental groups were submitted to intraperitoneal MCT inoculation (60 mg/kg) and were under its effect for 15, 30 and 37 days. The animals were then sacrificed, obtaining cardiac and hepatic tissues for anatomopathological and morphometric analysis. At macroscopic examination, the livers in the MCT groups presented a nutmeg-like appearance. PAH produced marked RVH and dilatation in the MCT groups, characterized by a significant increase in right ventricular free wall thickness (RVFWT) and chamber area. At histological evaluation, centrilobular congestion was the earliest manifestation, with preservation of the hepatocytes. Centrilobular hemorrhagic necrosis was observed in the groups exposed to prolonged MCT. Sinusoidal dilatation was markedly increased in the MCT groups, quantified by the Sinusoidal Lumen Ratio (SLR). The Congestive Hepatic Fibrosis Score and the Centrilobular Fibrosis Ratio (CFR) were also significantly increased in the MCT30 group. Hepatic atrophy, steatosis, apoptotic bodies and, rarely, hydropic swelling were also observed. SLR correlated strongly with CFR and RVFWT, and CFR correlated moderately with RVFWT. Our rat model was able to cause CH, related to monocrotaline-induced PAH and RVH; it was feasible, reproducible, and safe.

Can lightning strike twice? Wild-type transthyretin cardiac amyloidosis associated with rare liver disease

ABSTRACT Wild-type ATTR cardiac amyloidosis (ATTRwt-CA) is not as rare as previously thought to be. Patients with infiltrative cardiac amyloidosis often present with right-sided heart failure (HF) symptomatology. Clinically significant liver disease and cirrhosis has not been reported in ATTRwt-CA. We present two cases of ATTRwt-CA with right-sided HF and abnormal liver function tests initially thought to be secondary to congestive hepatopathy but found to have rare and unrelated liver disease. These cases highlight the importance of developing a broad differential diagnosis and leveraging a multidisciplinary team approach in evaluating patients for unusual causes of cirrhosis/other chronic liver diseases when ATTR cardiac amyloidosis patients present with congestive hepatopathy.

Overview on Cardiac Cirrhosis and Congestive Hepatopathy - A Review

Cardiac cirrhosis (congestive hepatopathy) refers to a group of hepatic abnormalities that develop as a result of right-sided heart failure. Cirrhosis of the liver can be induced by any right-sided pathology that leads to right-sided heart failure, which leads to increased venous congestion and pressure in the hepatic sinusoids. Because cardiac cirrhosis might be asymptomatic or diagnosed incorrectly due to other types of liver disease, determining its prevalence is difficult. The underlying heart disease, rather than the hepatic congestion and damage, is usually the cause of death in cardiac cirrhosis. The control of the underlying cardiac disease, as well as the optimization of cardiac output, are the mainstays of congestive hepatopathy treatment. Diuresis can help with hepatic congestion, but it must be used with caution to avoid causing hepatic ischemia. Hemodynamic therapy may be able to reverse the early stages of congestive hepatitis. The widespread use of heart transplantation (HT) and considerable breakthroughs in medical and surgical treatments have drastically altered the profile of CH patients. In this overview we will be looking at the disease cause, epidemiology, diagnosis, and treatment.

EXPRESS: Liver Abnormalities in Pulmonary Arterial Hypertension

Pulmonary arterial hypertension (PAH) is a cardio-pulmonary disease with high mortality. In recent years, it has been recognized that PAH is a multi-organ system disease involving, the systemic circulation, kidneys, skeletal muscles, and the central nervous system, amongst others. Right heart failure produces congestive hepatopathy, a disease state that has direct consequences on liver biochemistry, histology, and systemic glucose and lipid metabolism. This article aims to summarize the consequences of congestive hepatopathy with an emphasis on liver biochemistry, histology, and PAH-targeted therapy. Furthermore, PAH-specific changes in glucose and lipid metabolism will be discussed.