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Søren Møller - One of the best experts on this subject based on the ideXlab platform.
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the pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis
Liver International, 2018Co-Authors: Søren Møller, Flemming BendtsenAbstract:Patients with cirrhosis and portal hypertension often develop complications from a variety of organ systems leading to a multiple organ failure. The combination of liver failure and portal hypertension result in a hyperdynamic circulatory state partly owing to simultaneous splanchnic and peripheral arterial vasodilatation. Increases in circulatory vasodilators are believed to be due to portosystemic shunting and bacterial translocation leading to redistribution of the blood volume with central hypovolemia. Portal hypertension per se and increased splanchnic blood flow are mainly responsible for the development and perpetuation of the hyperdynamic circulation and the associated changes in cardiovascular function with development of Cirrhotic Cardiomyopathy, autonomic dysfunction, and renal dysfunction as part of a cardiorenal syndrome. Several of the cardiovascular changes are reversible after liver transplantation and point to the pathophysiological significance of portal hypertension. In this paper we aimed to review current knowledge on the pathophysiology of arterial vasodilatation and the hyperdynamic circulation in cirrhosis. This article is protected by copyright. All rights reserved.
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the pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis
Liver International, 2018Co-Authors: Søren Møller, Flemming BendtsenAbstract:Patients with cirrhosis and portal hypertension often develop complications from a variety of organ systems leading to a multiple organ failure. The combination of liver failure and portal hypertension results in a hyperdynamic circulatory state partly owing to simultaneous splanchnic and peripheral arterial vasodilatation. Increases in circulatory vasodilators are believed to be due to portosystemic shunting and bacterial translocation leading to redistribution of the blood volume with central hypovolemia. Portal hypertension per se and increased splanchnic blood flow are mainly responsible for the development and perpetuation of the hyperdynamic circulation and the associated changes in cardiovascular function with development of Cirrhotic Cardiomyopathy, autonomic dysfunction and renal dysfunction as part of a cardiorenal syndrome. Several of the cardiovascular changes are reversible after liver transplantation and point to the pathophysiological significance of portal hypertension. In this paper, we aimed to review current knowledge on the pathophysiology of arterial vasodilatation and the hyperdynamic circulation in cirrhosis.
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EDITORIAL Cardiopulmonary complications in chronic liver disease
2015Co-Authors: Søren Møller, Jens H Henriksen, Søren Møller Jens H HenriksenAbstract:Pat ients with c i rrhosis and porta l hypertension exhibit characteristic cardiovascular and pulmonary hemodynamic changes. A vasodilatatory state and a hyperdynamic circulation affecting the cardiac and pulmonary functions dominate the circulation. The recently defined Cirrhotic Cardiomyopathy may affect systolic and diastolic functions, and imply electromechanical abnormalities. In addition, the baroreceptor function and regulation of the circulatory homoeostasis is impaired. Pulmonary dysfunction involves diffusing abnormalities with the development of the hepatopulmonary syndrome and portopulmonary hypertension in some patients. Recent research has focused on the assertion that the hemodynamic an
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complications of cirrhosis a 50 years flashback
Scandinavian Journal of Gastroenterology, 2015Co-Authors: Søren Møller, Flemming BendtsenAbstract:In patients with cirrhosis and portal hypertension, it is largely the frequency and severity of complications relating to the diseased liver, degree of portal hypertension and hemodynamic derangement that determine the prognosis. It can be considered as a multiple organ failure that apart from the liver involves the heart, lungs, kidneys, the immune systems and other organ systems. Progressive fibrosis of the liver and subsequent metabolic impairment leads to a systemic and splanchnic arteriolar vasodilatation. With the progression of the disease development of portal hypertension leads to formation of esophageal varices and ascites. The circulation becomes hyperdynamic with cardiac, pulmonary as well as renal consequences for dysfunction and reduced survival. Infections and a changed cardiac function known as Cirrhotic Cardiomyopathy may be involved in further aggravation of other complications such as renal failure precipitating the hepatorenal syndrome. Patients with end-stage liver disease and related complications as for example the hepatopulmonary syndrome can only radically be treated by liver transplantation.
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Cirrhotic Cardiomyopathy a pathophysiological review of circulatory dysfunction in liver disease
Heart, 2002Co-Authors: Søren Møller, Jens H HenriksenAbstract:The systemic circulation in patients with cirrhosis is hyperdynamic with an increased cardiac output and heart rate and a reduced systemic vascular resistance as the most pronounced alterations. The concomitant cardiac dysfunction has recently been termed "Cirrhotic Cardiomyopathy", which is an entity different from that seen in alcoholic heart muscle disease. Clinically, these patients present with sodium fluid retention and strain often unmasks the presence of latent heart failure. No specific treatment can yet be recommended but caution should be used with respect to procedures that may stress the heart such as shunt implantation and liver transplantation.
Flemming Bendtsen - One of the best experts on this subject based on the ideXlab platform.
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the pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis
Liver International, 2018Co-Authors: Søren Møller, Flemming BendtsenAbstract:Patients with cirrhosis and portal hypertension often develop complications from a variety of organ systems leading to a multiple organ failure. The combination of liver failure and portal hypertension result in a hyperdynamic circulatory state partly owing to simultaneous splanchnic and peripheral arterial vasodilatation. Increases in circulatory vasodilators are believed to be due to portosystemic shunting and bacterial translocation leading to redistribution of the blood volume with central hypovolemia. Portal hypertension per se and increased splanchnic blood flow are mainly responsible for the development and perpetuation of the hyperdynamic circulation and the associated changes in cardiovascular function with development of Cirrhotic Cardiomyopathy, autonomic dysfunction, and renal dysfunction as part of a cardiorenal syndrome. Several of the cardiovascular changes are reversible after liver transplantation and point to the pathophysiological significance of portal hypertension. In this paper we aimed to review current knowledge on the pathophysiology of arterial vasodilatation and the hyperdynamic circulation in cirrhosis. This article is protected by copyright. All rights reserved.
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the pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis
Liver International, 2018Co-Authors: Søren Møller, Flemming BendtsenAbstract:Patients with cirrhosis and portal hypertension often develop complications from a variety of organ systems leading to a multiple organ failure. The combination of liver failure and portal hypertension results in a hyperdynamic circulatory state partly owing to simultaneous splanchnic and peripheral arterial vasodilatation. Increases in circulatory vasodilators are believed to be due to portosystemic shunting and bacterial translocation leading to redistribution of the blood volume with central hypovolemia. Portal hypertension per se and increased splanchnic blood flow are mainly responsible for the development and perpetuation of the hyperdynamic circulation and the associated changes in cardiovascular function with development of Cirrhotic Cardiomyopathy, autonomic dysfunction and renal dysfunction as part of a cardiorenal syndrome. Several of the cardiovascular changes are reversible after liver transplantation and point to the pathophysiological significance of portal hypertension. In this paper, we aimed to review current knowledge on the pathophysiology of arterial vasodilatation and the hyperdynamic circulation in cirrhosis.
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complications of cirrhosis a 50 years flashback
Scandinavian Journal of Gastroenterology, 2015Co-Authors: Søren Møller, Flemming BendtsenAbstract:In patients with cirrhosis and portal hypertension, it is largely the frequency and severity of complications relating to the diseased liver, degree of portal hypertension and hemodynamic derangement that determine the prognosis. It can be considered as a multiple organ failure that apart from the liver involves the heart, lungs, kidneys, the immune systems and other organ systems. Progressive fibrosis of the liver and subsequent metabolic impairment leads to a systemic and splanchnic arteriolar vasodilatation. With the progression of the disease development of portal hypertension leads to formation of esophageal varices and ascites. The circulation becomes hyperdynamic with cardiac, pulmonary as well as renal consequences for dysfunction and reduced survival. Infections and a changed cardiac function known as Cirrhotic Cardiomyopathy may be involved in further aggravation of other complications such as renal failure precipitating the hepatorenal syndrome. Patients with end-stage liver disease and related complications as for example the hepatopulmonary syndrome can only radically be treated by liver transplantation.
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Splanchnic and Systemic Haemodynamic Derangement in Decompensated Cirrhosis
Hindawi Limited, 2001Co-Authors: Søren Møller, Flemming Bendtsen, Jens H HenriksenAbstract:Patients with cirrhosis and portal hypertension exhibit characteristic hemodynamic changes with hyperkinetic systemic circulation, abnormal distribution of blood volume and neurohumoral dysregulation. Their plasma and noncentral blood volumes are increased. Splanchnic vasodilation is of pathogenic significance to the low systemic vascular resistance and abnormal volume distribution of blood, which are important elements in the development of the concomitant cardiac dysfunction, recently termed 'Cirrhotic Cardiomyopathy'. Systolic and diastolic functions are impaired with direct relation to the degree of liver dysfunction. Significant pathophysiological mechanisms are reduced beta-adrenergic receptor signal transduction, defective cardiac excitation-contraction coupling and conductance abnormalities. Vasodilators such as nitric oxide and calcitonin gene-related peptide are among the candidates in vasodilation and increased arterial compliance. Reflex-induced, enhanced sympathetic nervous system activity, activation of the renin-angiotensin aldosterone system, and elevated circulation vasopressin and endothelin-1 are implicated in hemodynamic counter-regulation in cirrhosis. Recent research has focused on the assertion that the hemodynamic and neurohumoral abnormalities in cirrhosis are part of a general cardiovascular dysfunction, influencing the course of the disease with the reduction of organ function, with sodium and water retention as the outcome. These aspects are relevant to therapy
Paolo Angeli - One of the best experts on this subject based on the ideXlab platform.
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easl clinical practice guidelines for the management of patients with decompensated cirrhosis
Journal of Hepatology, 2018Co-Authors: Paolo Angeli, M Bernardi, Candid Villanueva, Claire Francoz, Rajeshwar P Mookerjee, Jonel Trebicka, Aleksander Krag, Wim Laleman, Pere GinesAbstract:Summary The natural history of cirrhosis is characterised by an asymptomatic compensated phase followed by a decompensated phase, marked by the development of overt clinical signs, the most frequent of which are ascites, bleeding, encephalopathy, and jaundice. The following Clinical Practice Guidelines (CPGs) represent the first CPGs on the management of decompensated cirrhosis. In this context, the panel of experts, having emphasised the importance of initiating aetiologic treatment for any degree of hepatic disease at the earliest possible stage, extended its work to all the complications of cirrhosis, which had not been covered by the European Association for the Study of the Liver guidelines, namely: ascites, refractory ascites, hyponatremia, gastrointestinal bleeding, bacterial infections, acute kidney injury, hepatorenal syndrome, acute-on-chronic liver failure, relative adrenal failure, Cirrhotic Cardiomyopathy, hepatopulmonary syndrome, and porto-pulmonary hypertension. The panel of experts, produced these GPGs using evidence from PubMed and Cochrane database searches providing up to date guidance on the management of decompensated cirrhosis with the only purpose of improving clinical practice.
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an abnormal gene expression of the β adrenergic system contributes to the pathogenesis of Cardiomyopathy in Cirrhotic rats
Hepatology, 2008Co-Authors: Giulio Ceolotto, Italia Papparella, A Sticca, Sergio Bova, Maurizio Cavalli, Gabriella Cargnelli, Andrea Semplicini, Angelo Gatta, Paolo AngeliAbstract:Decreased cardiac contractility and β-adrenergic responsiveness have been observed in Cirrhotic Cardiomyopathy, but their molecular mechanisms remain unclear. To study β-adrenergic–stimulated contractility and β-adrenergic gene expression patterns, 20 Wistar Kyoto rats were treated with carbon tetrachloride to induce cirrhosis and 20 rats were used as controls. Left ventricular contractility was recorded in electrically driven isolated hearts perfused at constant flow with isoproterenol (10−10 to 10−6 M). A cardiac gene expression profile was obtained using a microarray for the myocyte adrenergic pathway. The cardiac contractility maximal response to isoproterenol was significantly reduced in Cirrhotic rats in comparison to control rats, whereas the half-maximal effective concentration was not different. In Cirrhotic rats, cardiac gene expression analysis showed a significant overexpression of G protein alpha–inhibiting subunit 2 (Gαi2), cyclic nucleotide phosphodiesterase (PDE2a), regulator of G-protein signaling 2 (RGS2), and down-expression of adenylate cyclase (Adcy3). These results indicate that overexpression of Gαi2, PDE2a, and RGS2 down-regulates the β-adrenergic signaling pathway, thus contributing to the pathogenesis of Cirrhotic Cardiomyopathy. (HEPATOLOGY 2008;48:1913-1923.)
Catherine Williamson - One of the best experts on this subject based on the ideXlab platform.
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heart and bile acids clinical consequences of altered bile acid metabolism
Biochimica et Biophysica Acta, 2018Co-Authors: Tharni Vasavan, Elisa Ferraro, Effendi Ibrahim, Peter H Dixon, Julia Gorelik, Catherine WilliamsonAbstract:Abstract Cardiac dysfunction has an increased prevalence in diseases complicated by liver cirrhosis such as primary biliary cholangitis and primary sclerosing cholangitis. This observation has led to research into the association between abnormalities in bile acid metabolism and cardiac pathology. Approximately 50% of liver cirrhosis cases develop Cirrhotic Cardiomyopathy. Bile acids are directly implicated in this, causing QT interval prolongation, cardiac hypertrophy, cardiomyocyte apoptosis and abnormal haemodynamics of the heart. Elevated maternal serum bile acids in intrahepatic cholestasis of pregnancy, a disorder which causes an impaired feto-maternal bile acid gradient, have been associated with fatal fetal arrhythmias. The hydrophobicity of individual bile acids in the serum bile acid pool is of relevance, with relatively lipophilic bile acids having a more harmful effect on the heart. Ursodeoxycholic acid can reverse or protect against these detrimental cardiac effects of elevated bile acids.
Giacomo Zaccherini - One of the best experts on this subject based on the ideXlab platform.
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qt interval prolongation in liver cirrhosis innocent bystander or serious threat
Expert Review of Gastroenterology & Hepatology, 2012Co-Authors: Mauro Bernardi, Caterina Maggioli, Valmir Dibra, Giacomo ZaccheriniAbstract:The ECG QT interval measures the length of ventricular systole. Its prolongation is essentially caused by a delayed repolarization phase, and is associated with an increased risk of ventricular arrhythmias and sudden death in several congenital and acquired conditions. Abnormalities in cardiac electrophysiology are well documented in patients with liver cirrhosis, and the prolonged QT interval has emerged as the electrophysiological hallmark of Cirrhotic Cardiomyopathy. This article will focus on: first, the epidemiology of QT interval prolongation in cirrhosis; second, the potential molecular mechanisms responsible for the pathogenesis of this electrophysiological abnormality and the putative role of circulating cardiotoxins; third, its prognostic meaning; and fourth, its clinical relevance, in terms of the association between the presence of a long QT interval and the occurrence of ventricular arrhythmias in Cirrhotic patients treated with drugs known to increase the QT length or exposed to stressful co...