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Heart Failure Reviews

, Volume 21, Issue 5, pp 599–610 | Cite as

Diastolic dysfunction in cirrhosis

  • Søren MøllerEmail author
  • Signe Wiese
  • Hanne Halgreen
  • Jens D. Hove
Article

Abstract

Development of esophageal varices, ascites, and hepatic nephropathy is among the major complications of cirrhosis. The presence of cirrhotic cardiomyopathy, which includes a left ventricular diastolic dysfunction (DD), seems to deteriorate the course of the disease and the prognosis. Increased stiffness of the cirrhotic heart may decrease the compliance and result in DD. The prevalence of DD in cirrhotic patients averages about 50 %. It can be evaluated by transmitral Doppler echocardiography, tissue Doppler echocardiography, and cardiac magnetic resonance imaging. There seems to be a relation between DD and the severity of liver dysfunction and the presence of ascites. After liver transplantation, DD worsens the prognosis and increases the risk of graft rejection, but DD improves after few months. Insertion of a transjugular intrahepatic portosystemic shunt increases left ventricular diastolic volumes, and DD is a predictor of poorer survival in these patients. Future studies should aim at disclosing pathophysiological mechanisms behind the developing of DD in cirrhosis in relation to patient characteristics, development of complications, treatment, and risk associated with interventional procedures.

Keywords

Cirrhotic cardiomyopathy Hyperdynamic syndrome Systolic dysfunction Cardiac dysfunction Vasodilatation 

Abbreviations

AC

Atrial contribution

ANP

Atrial natriuretic peptide

BNP

Brain natriuretic peptide

BRS

Baroreflex sensitivity

CGRP

Calcitonin gene-related peptide

CMR

Cardiac magnetic resonance imaging

DD

Left ventricular diastolic dysfunction

DDT

Diastolic deceleration time

IL

Interleukin

IR

Isovolumetric relaxation phase

IVRT

Isovolumetric relaxation time

LVEF

Left ventricular ejection fraction

MELD

Model of end-stage liver disease

PICD

Post-paracentesis-induced circulatory dysfunction

RAAS

Renin–angiotensin–aldosterone system

RF

Rapid filling

SF

Slow filling

TIPS

Transjugular portosystemic shunt

TNF

Tumor necrosis factor

Notes

Acknowledgments

SM received a research grant from the Novo Nordisk Foundation.

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Copyright information

© Springer Science+Business Media New York 2016

Authors and Affiliations

  • Søren Møller
    • 1
    Email author
  • Signe Wiese
    • 1
  • Hanne Halgreen
    • 1
  • Jens D. Hove
    • 2
  1. 1.Department of Clinical Physiology and Nuclear Medicine 260, Centre for Functional Imaging and Research, Faculty of Health Sciences, Hvidovre HospitalUniversity of CopenhagenCopenhagenDenmark
  2. 2.Department of Cardiology, Faculty of Health Sciences, Hvidovre HospitalUniversity of CopenhagenCopenhagenDenmark

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