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See Commentary, p 1167
Linked articles242511.
Significance of the study
What is already known about this subject?
Cirrhosis and portal hypertension are associated with abnormal haemodynamic homeostasis with a hyperdynamic circulation.
Results of experimental studies support augmented shear stress-induced splanchnic inflow to play a role in the systemic haemodynamic changes.
Development of extrahepatic complications affects the prognosis of the patients.
What are the new findings?
Changes in pertinent systemic haemodynamics including those reflecting the hyperdynamic circulation and central hypovolaemia are determined by changes in hepatic blood flow.
Changes in cardiac function affect survival.
One factor in a principal component analysis included aspects of cardiac preload and this factor had prognostic value.
How might it impact on clinical practice in the foreseeable future?
Increase our knowledge and understanding of the link between the liver and systemic haemodynamic changes in cirrhosis.
Focus the clinicians on the importance of the splanchnic haemodynamic changes for the development of extrahepatic complications and in particular cardiac dysfunction.
Identification of new prognostic variables may contribute to optimise the patient management.
Introduction
Patients with cirrhosis have a generalised circulatory dysfunction with abnormalities in the splanchnic as well as in the systemic circulation.1 2 Increased post-sinusoidal resistance (PSR) together with increased splanchnic inflow lead to portal hypertension, which gives rise to a number of complications such as formation of oesophageal varices, ascites, hepatic encephalopathy, and the hepatorenal syndrome.3 4 In addition, patients with cirrhosis exhibit a systemic hyperdynamic circulation that includes an increased cardiac output (CO) and heart rate (HR) and reduced systemic arterial blood pressure (BP) and systemic vascular resistance (SVR).5 6 Although the changes in the splanchnic and systemic haemodynamics appear simultaneously, the link between these haemodynamic alterations is still unknown and the initiating mechanism(s) responsible for the development of the hyperdynamic circulation and central hypovolaemia are still to be resolved. There is now a general consensus of a preferential splanchnic arterial vasodilatation as one of the pathophysiological hallmarks in cirrhosis.7 Various experimental studies indicate that shear stress in the splanchnic circulation elicited by changes in hepatic blood flow (HBF) contributes to this phenomenon.8–11
The aim of the present study was therefore in a large population of patients with cirrhosis with various degrees of severity of...





