Echocardiographic findings before and after liver transplantation

doi:10.1016/0002-9149(85)90507-7

The American Journal of Cardiology

Volume 55, Issue 11, 1 May 1985, Pages 1373-1378

https://doi.org/10.1016/0002-9149(85)90507-7 Get rights and content

Abstract

Echocardiographic studies were performed in 73 patients with various types of chronic liver disease. They were 0.5 to 19 years old (mean 5). Thirteen patients underwent follow-up echocardiography 1 to 13 months (mean 6) after liver transplantation. Preoperatively 60 patients (82%) showed evidence of high cardiac output (cardiac index greater than 4 liters/min/m²); these patients manifested increased left ventricular (LV) and left atrial dimensions and a thickened LV posterior wall. Transvenous contrast echocardiographic study confirmed the presence of intrapulmonary arteriovenous shunting in 4 patients. Studies after liver transplantation revealed a reduced LV end-diastolic dimension in 12 patients. Cardiac index was reduced a mean of 35% after transplantation (p < 0.001). This study suggests that liver transplantation improves common hemodynamic abnormalities in chronic liver disease.

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Cited by (41)

A detailed evaluation of cardiac function in cirrhotic patients and its alteration with or without liver transplantation
2016, Journal of Cardiology
Citation Excerpt :
Nonetheless studies of RV function in these patients compared with controls are scarce. Further, only limited studies have prospectively evaluated the altered myocardial function in patients with cirrhosis and assessed the changes following LTx [7,8]. Therefore the aim of the present study was to compare the LV and RV (biventricular) function in cirrhotic patients with controls and prospectively evaluate the difference in progression of biventricular function in cirrhotic patients with and without LTx.
Cirrhosis has been shown to be associated with left ventricular (LV) myocardial dysfunction, but studies of right ventricular (RV) function in cirrhotic patients compared with controls are scarce. Limited studies have prospectively evaluated the progression of myocardial function in patients with cirrhosis and assessed changes in cardiac function following liver transplantation (LTx). So the aim of the study was to evaluate biventricular myocardial function in cirrhotic patients and its alteration with or without liver transplantation.
A total of 103 patients with cirrhosis (age 55 ± 7 years, male 75%) were recruited. Conventional and 2-dimensional speckle tracking echocardiography was performed to determine the presence of LV and RV (biventricular) dysfunction. For comparison, 48 matched control subjects were included. Follow-up echocardiography was performed in 41 patients following LTx and in 26 patients who did not undergo LTx.
Patients with cirrhosis had biventricular dilatation, increased LV mass, impaired LV diastolic function, and biventricular systolic strain compared with controls. Following LTx, cirrhotic patients had reduced biventricular dilatation, a smaller LV mass, and improved biventricular systolic strain after a mean duration of 18.2 ± 6.6 months. Patients who did not undergo LTx had a further increase in LV mass but no significant change in biventricular dimensions or systolic strain (mean duration of 20.4 ± 8.3 months).
The present study demonstrates that patients with cirrhosis had biventricular dilatation and impaired biventricular systolic strain compared with controls. Following LTx, biventricular dilatation reduced and biventricular systolic strain improved. In contrast, patients who did not undergo LTx experienced a further increase in LV mass.
Cardiovascular Complications of Cirrhosis
2012, Zakim and Boyer's Hepatology
Clinical Consequences of Liver Disease: Cardiovascular
2006, Zakim and Boyer's Hepatology
The pulmonary involvement in portal hypertension: Portopulmonary hypertension and hepatopulmonary syndrome
2006, Gastroenterologia y Hepatologia
Pulmonary abnormalities are common in patients with advanced chronic liver disease. Two distinct syndromes strictly related to the presence of portal hypertension, but clearly different from a pathophysiologic point of view, have been identified. Portopulmonary hypertension, characterized by an increased pulmonary arterial pressure, is due to a progressive arteriolar vasoconstriction induced by excess local production of vasoconstrictor substances. Hepatopulmonary syndrome results from intrapulmonary microvascular dilation caused by an inadequate synthesis or metabolism of putative pulmonary vasoactive substances leading to a functional vasodilation of the pulmonary vasculature, ultimately leading to hypoxemia. Controversies on pathogenesis imply different tentative therapeutic approaches for the medical menagement of these conditions. The development of portopulmonary hypertension or the hepatopulmonary syndrome has important clinical and prognostic implications facing the impact of new therapeutic strategies for the menagement of the main complications of advanced liver diseases on cardiopulmonary function.
Las alteraciones pulmonares son frecuentes en los pacientes con hepatopatía crónica avanzada. Se han identificado 2 síndromes específicos relacionados de manera estricta con la presencia de hipertensión portal, pero que son claramente diferentes desde el punto de vista fisiopatológico. La hipertensión portopulmonar, caracterizada por el incremento de la presión en la arteria pulmonar, se debe a un proceso de vasoconstricción arteriolar progresiva inducido por la producción local excesiva de sustancias vasoconstrictoras. El síndrome hepatopulmonar se debe a la dilatación microvascular intrapulmonar secundaria a la síntesis o el metabolismo inadecuados de posibles sustancias vasoactivas pulmonares, con un cuadro de vasodilatación funcional de la vasculatura pulmonar que, en última instancia, causa hipoxemia. Las controversias relativas a la patogenia se deben a la existencia de diferentes abordajes terapéuticos en el tratamiento médico de estos procesos. El desarrollo de la hipertensión portopulmonar o del síndrome hepatopulmonar tiene implicaciones clínicas y pronósticas importantes respecto del impacto de las nuevas estrategias terapéuticas utilizadas en el tratamiento de las complicaciones principales que las hepatopatías avanzadas inducen en la función pulmonar.
Hepatopulmonary syndrome: A good relationship gone bad
2003, Gastroenterology
Occurrence of hepatopulmonary syndrome in Budd-Chiari syndrome and the role of venous decompression
2002, Gastroenterology
Citation Excerpt :
Of the patients with negative CE, 1 died due to uncontrolled variceal bleeding and another due to the associated retroperitoneal spindle cell sarcoma. HPS has been reported predominantly in cirrhotic patients,7 with the incidence of positive CE varying from 5% to 47%19,20 and prevalence of HPS between 5% and 29%.18,21 Rarely does HPS develop in cases of noncirrhotic portal hypertension,8–12 and reports in cases of BCS are purely anecdotal.10,12
Background & Aims: Hepatopulmonary syndrome (HPS) has been predominantly detected in cirrhotic patients and rarely in patients with noncirrhotic portal hypertension. The aim of this study was to determine the occurrence of HPS in patients with Budd–Chiari syndrome (only anecdotal reports available) and evaluate the role of venous decompression in its reversal. Methods: Twentynine consecutive cases of Budd–Chiari syndrome without primary cardiopulmonary disease were investigated by air contrast echocardiography and arterial blood gas analysis. Venous decompression (e.g., by balloon cavoplasty) was attempted when feasible. Results: Eight cases (27.6%) of HPS and 9 cases (31.0%) with positive contrast echocardiography but unimpaired oxygenation were detected. Duration of disease was longer (P = 0.026) among those with positive contrast echocardiography. Cavoplasty reversed 4 of 5 cases of HPS and 2 of 2 cases with positive contrast echocardiography alone. Venous decompression by drainage of amebic liver abscess (which was compressing hepatic venous outflow) also reversed 1 case of HPS. HPS was relieved by venous decompression in 5 of 6 cases. Conclusions: HPS developed in a substantial fraction of our patients with Budd–Chiari syndrome, with positive contrast echocardiography occurring mainly in the benign, slowly progressing variety. Venous decompression showed promise in reversing such cases.
GASTROENTEROLOGY 2002;122:897-903

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Echocardiographic findings before and after liver transplantation

Abstract

J Pediatr

Am J Med

J Pediatr

Pediatrics

Am J Cardiol

Syndrome of intrahepatic biliary dysgenesis and cardiovascular malformation

J Pediatr

Arteriohepatic dysplasia: familial pulmonary arterial stenosis with neonatal liver disease

Arch Dis Child

Recommendations regarding quantitation in M-mode electrocardiography: results of a survey of echo-cardiographic measurements

Circulation

Ultrasonic cardiac echocardiography for determining stroke volume and valve regurgitation

Circulation