Altered cardiovascular responsiveness to active tilting in nonalcoholic cirrhosis
Abstract
BACKGROUND & AIMS: The hyperdynamic circulation of cirrhosis has been related either to plasma volume expansion (increased preload) or peripheral arterial vasodilation (reduced afterload). The aim of this study was to evaluate cardiovascular function in patients with nonalcoholic cirrhosis by echocardiography. METHODS: Nineteen patients with abnormal sodium handling (11 sodium excretors and 8 sodium retainers) and 15 healthy volunteers underwent echocardiographic evaluation of left ventricular end-diastolic volume index (LVEDVI) and left ventricular end-systolic volume index (LVESVI), left ventricular ejection fraction (LVEF), cardiac index (CI), mean arterial pressure, and systemic vascular resistance (SVR) during supine resting and after 5 minutes of standing. RESULTS: Supine patients had increased LVEF and CI and reduced LVESVI and SVR. LVEDVI was increased only in sodium excretors. Standing induced a decrease in LVEDVI in all subjects. Healthy volunteers maintained cardiovascular homeostasis by increasing LVEF and heart rate, whereas cirrhotic patients experienced a decrease in SVI and CI despite marked increments in heart rate, plasma renin activity, and plasma norepinephrine level. CONCLUSIONS: In patients with cirrhosis, the increased LVEF and reduced LVESVI while in a supine position point at reduced afterload as an important determinant of the hyperdynamic circulation. Evidence of an increased preload secondary to increased blood volume, indicated by a high LVEDVI and increased plasma atrial natriuretic peptide levels, was found only in sodium excretors. The altered response to active tilt in cirrhotic patients suggests an impaired myocardial contractility. (Gastroenterology 1997 Sep;113(3):891-8)
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A Prospective Study of Prevalence and Predictors of Cirrhotic Cardiomyopathy and Its Role in Development of Hepatorenal Syndrome
2022, Journal of Clinical and Experimental HepatologyCitation Excerpt :This was possibly due to the small number of patients who underwent DSE and the relatively compensated patients in the evaluated cohort. There are many studies in literature which have reported systolic cardiac dysfunction in patients with cirrhosis.26–28 Wong et al.24 demonstrated an abnormal and inverse systolic pressure to end-systolic volume relationship, an index of myocardial contractility in both alcoholic and nonalcoholic cirrhotic patients, with or without ascites.
Cirrhotic cardiomyopathy (CCM) is a term used to collectively describe abnormal structural and functional changes in heart of patients with cirrhosis. The present study was undertaken to find the prevalence of CCM in patients with liver cirrhosis and its predictors. We also followed these patients to evaluate the role of CCM in the development of hepatorenal syndrome (HRS).
This was a prospective study carried out in department of Gastroenterology, Sir Ganga Ram hospital, New Delhi. A total of 104 patients with liver cirrhosis were included. Liver cirrhosis was diagnosed on basis of clinical, biochemical, and imaging features. CCM was defined based on echocardiography. Dobutamine stress echocardiography and hepatic venous pressure gradient (HVPG) were performed in patients who gave consent. HRS was defined as per standard criteria. Patients with CCM were followed for development of HRS.
Fifty (48%) patients were diagnosed with CCM. All patients had diastolic dysfunction, and none had systolic dysfunction. Median age of patients with CCM was significantly higher (59 [31–78 y] vs. 52 [24–70 y], P < 0.05). Severity of liver disease (Child Turcotte Pugh score and model for end-stage liver disease score) and portal pressures (HVPG) did not differ in patients with or without CCM. Patients with CCM did not have increased incidence of HRS at the end of 6-month follow-up study.
The presence of CCM was not related with the severity of liver dysfunction or portal pressures. Age was a significant determinant of CCM. Diastolic cardiac dysfunction does not influence the occurrence of HRS.
Myocardial Dysfunction in Cirrhotic Cardiomyopathy is Associated with Alterations of Phospholamban Phosphorylation and IL-6 Levels
2021, Archives of Medical ResearchDecreased cardiac contractility has been observed in cirrhosis, but the mechanisms that initiate and maintain cardiac dysfunction are not entirely understood.
Aim of the study. We test the hypothesis that cirrhotic cardiomyopathy is related to deterioration of myocardial contractility due to alterations in calcium-handling proteins expression. In addition, we evaluated whether cardiac pro-inflammatory cytokine levels are associated with this process.
Cirrhosis was induced by thioacetamide (TAA, 100 mg/kg/i.p., twice weekly for eight weeks). The myocardial performance was evaluated in isolated left ventricle papillary muscles under basal conditions and after inotropic challenge. The cardiac calcium handling protein expression was detected by Western blotting. Cardiac TNF-α and IL-6 levels were measured by ELISA.
Thioacetamide induced liver cirrhosis, which was associated with cirrhotic cardiomyopathy characterized by in vivo left ventricular diastolic and systolic dysfunction as well as cardiac hypertrophy. In vitro baseline myocardial contractility was lower in cirrhosis. Also, myocardial responsiveness to post-rest contraction stimulus was declined. Protein expression for RYR2, SERCA2, NCX, pPBL Ser16 and L-type calcium channel was quantitatively unchanged; however, pPBL Thr17 was significantly lower while IL-6 was higher.
Our study demonstrates that cirrhotic cardiomyopathy is associated with decreased cardiac contractility with alteration of phospholamban phosphorylation in association with higher cardiac pro-inflammatory IL-6 levels. These findings provided molecular and functional insights about the effects of liver cirrhosis on cardiac function.
Takotsubo Cardiomyopathy Resulting in Cardiac Arrest in a Patient Undergoing Liver Transplantation
2017, Transplantation ProceedingsCardiac complications during and after liver transplantation are a common cause of death. Although considered to be uncommon, takotsubo cardiomyopathy, which is characterized by reversible left ventricular akinesis without coronary artery obstruction, is becoming increasingly reported. Herein we have presented a case of reversible stress-induced takotsubo cardiomyopathy resulting in cardiac arrest in a patient undergoing liver transplantation.
Cirrhotic cardiomyopathy: A specific entity
2012, Annales de Cardiologie et d'AngeiologieLa cirrhose, stade ultime de nombreuses hépatopathies chroniques, est une pathologie fréquente et sévère. Elle est associée à des perturbations hémodynamiques majeures définissant la circulation hyperdynamique, et peut se compliquer d’une atteinte cardiaque spécifique, ou cardiomyopathie cirrhotique, dont la physiopathologie est multifactorielle. Celle-ci associe des anomalies morphologiques, fonctionnelles, électrophysiologiques et biologiques d’autant plus sévères que la pathologie hépatique est avancée. À l’état de base, l’effondrement de la postcharge lié à la circulation hyperdynamique permet de pallier à cette défaillance cardiaque latente. Cependant, une variation brutale des conditions hémodynamiques (remplissage vasculaire agressif, création de shunts portocaves par voie endovasculaire ou chirurgicale, dérivations péritonéojugulaires, transplantation hépatique) ou une diminution de la contractilité intrinsèque ventriculaire gauche (notamment lors de l’introduction d’un traitement bêtabloquant) peut déstabiliser cet équilibre, précipitant alors l’apparition d’une insuffisance cardiaque. La cardiomyopathie cirrhotique serait également impliquée dans la genèse du syndrome hépatorénal, expression extrême de la dysfonction circulatoire liée à la cirrhose. Les critères diagnostiques de cette entité décrite récemment restent à préciser. À ce jour, elle ne relève d’aucun traitement spécifique. L’éventualité d’une telle cardiopathie chez le cirrhotique impose la prudence au clinicien, avant, pendant et après toute intervention à risque.
Cirrhosis is a frequent and severe condition, which is the late stage of numerous chronic liver diseases. It is associated with major hemodynamic alterations characteristic of hyperdynamic circulation and with a series of structural, functional, electrophysiological and biological heart abnormalities termed cirrhotic cardiomyopathy. The pathogenesis of this syndrome is multifactorial. It is usually clinically latent or mild, likely because the peripheral vasodilatation significantly reduces the left ventricle afterload. However, sudden changes of hemodynamic state (vascular filling, surgical or transjugular intrahepatic porto-systemic shunts, peritoneo-venous shunts and orthotopic liver transplantation) or myocardial contractility (introduction of beta-blocker therapy) can unmask its presence, and sometimes convert latent to overt heart failure. Cirrhotic cardiomyopathy may also contribute to the pathogenesis of hepatorenal syndrome. This entity has been described recently, and its diagnostic criteria are still under debate. To date, current management recommendations are empirical, nonspecific measures. Recognition of cirrhotic cardiomyopathy depends on a high level of awareness for the presence of this syndrome, particularly in patients with advanced cirrhosis who undergo significant surgical, pharmacological or physiological stresses.
Elevated plasma levels of urotensin II do not correlate with systemic haemodynamics in patients with cirrhosis
2011, Digestive and Liver DiseaseThe hyperdynamic circulation of hepatic cirrhosis is related to decreased systemic vascular resistance due to arterial vasodilation. Urotensin II plasma levels are increased in cirrhotic patients, and have been suggested to play a role in the pathogenesis of systemic haemodynamic alterations.
To evaluate the relationships between systemic haemodynamics and urotensin II plasma levels.
Thirty-six consecutive in-patients with cirrhosis and no alteration of plasma creatinine, and 20 age- and gender-matched healthy volunteers underwent noninvasive assessment of systemic haemodynamics and measurement of urotensin II plasma levels.
In comparison to healthy controls, cirrhotic patients had signs of hyperdynamic circulation and higher plasma urotensin II levels. Plasma urotensin II was neither significantly different amongst patients with different severity of cirrhosis nor between patients with or without ascites. Both in controls and cirrhotic patients no significant correlations were found between parameters of systemic haemodynamics and plasma urotensin II levels.
In patients with cirrhosis and hyperdynamic circulation, but with normal serum creatinine, urotensin II is higher than in healthy subjects. However, no correlation with cardiac index or other haemodynamic parameters was observed, indicating that other mechanisms prevail.
The heart in liver transplantation
2011, Journal of HepatologyThe heart and liver are organs that are closely related in both health and disease. Patients who undergo liver transplantation may suffer from heart disease that is: (a) related to the original cause of the liver disease such as hemochromatosis, (b) related to the liver disease itself, or (c) related to other associated conditions. Furthermore, liver transplantation is one of the most cardiovascular stressful events that a patient with cirrhosis may undergo. After liver transplantation, the progression of pre-existing or the development of new-onset cardiac disease may occur. This article reviews the relationship between the heart and liver transplantation in the pre-transplant, intra-operative, and post-transplant periods.