Ascites in Animals With Right Heart Failure: Correlation With Lymphatic Dysfunction

Background Congestive heart failure is a leading cause of morbidity and mortality worldwide. One of the signs of congestive heart failure is fluid overload including pulmonary edema, peripheral edema, and ascites. The cause of fluid overload remains incompletely understood, and management of these patients continues to be a challenge. The role of lymphatic circulation abnormalities in the cause and pathophysiology of fluid overload also remains unclear. Here we report on a study in a large animal model of right heart failure caused by severe tricuspid regurgitation comparing cardiovascular and lymphatic findings in a group of animals that did not develop ascites with a group of animals that developed ascites. Methods and Results Thirteen Yorkshire pigs were included in this study divided into 2 groups. Group 1 included 6 animals that did not develop ascites, and Group 2 included 7 animals that had developed ascites. The groups were compared on hemodynamic parameters as well as comparison of the animal's lymphatic anatomy and function. There was no difference between the groups in degree of tricuspid regurgitation and central venous pressure, with inferior vena cava pressure measuring 11.6±1.6 versus 13.2±3.7 (P=0.534) and superior vena cava pressure measuring 12.0±2.3 versus 13.7±3.2 (P=0.366). There was also no difference between the groups in all measured hemodynamic parameters, including right ventricular pressure, pulmonary artery pressure, and left ventricular function. The weighted liver size in the ascites group was significantly larger than in the nonascites group (30.3±12.4 versus 63.3±14.0 mL/kg, respectively; P=0.001). The 2 groups also differed in the number of animals with regurgitant thoracic duct flow (Group 1: 1/6,17% versus Group 2: 6/7, 86%; P=0.029) and the minimal thoracic duct diameter (Group 1: 2.3±0.3 versus Group 2: 4.2±2.2; P=0.035). Conclusions In animals with right heart failure caused by severe tricuspid regurgitation, fluid overload did not correlate with hemodynamic parameters but rather with changes in the lymphatic system, including regurgitant lymphatic flow, minimal thoracic duct diameter, and liver size. This study is consistent with lymphatic dysfunction and not cardiovascular function playing a significant role in the cause of fluid overload. Further studies are needed to confirm these findings.