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Cirrhotic cardiomyopathy.
J Hepatol. 2010 Jul; 53(1):179-90.JH

Abstract

Increased cardiac output was first described in patients with cirrhosis more than fifty years ago. Later, various observations have indicated the presence of a latent cardiac dysfunction, which includes a combination of reduced cardiac contractility with systolic and diastolic dysfunction and electrophysiological abnormalities. This syndrome is termed cirrhotic cardiomyopathy. Results of experimental studies indicate the involvement of several mechanisms in the pathophysiology, such as reduced beta-adrenergic receptor signal transduction, altered transmembrane currents and electromechanical coupling, nitric oxide overproduction, and cannabinoid receptor activation. Systolic incompetence in patients can be revealed by pharmacological or physical strain and during stressful procedures, such as transjugular intrahepatic portosystemic shunt insertion and liver transplantation. Systolic dysfunction has recently been implicated in development of renal failure in advanced disease. Diastolic dysfunction reflects delayed left ventricular filling and is partly attributed to ventricular hypertrophy, subendocardial oedema, and altered collagen structure. The QT interval is prolonged in about half of the cirrhotic patients and it may be normalised by beta-blockers. No specific therapy for cirrhotic cardiomyopathy can be recommended, but treatment should be supportive and directed against the cardiac dysfunction. Future research should better describe the prevalence, impact on morbidity and survival, and look for potential treatments.

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Authors+Show Affiliations

Møller S
Department of Clinical Physiology and Nuclear Medicine, Hvidovre Hospital, Faculty of Health Sciences, University of Copenhagen, Denmark. soeren.moeller@hvh.regionh.dk
Henriksen JH
No affiliation info available

MeSH

AnimalsBaroreflexCalcium SignalingCardiomyopathiesElectrocardiographyHumansLiver CirrhosisLiver TransplantationModels, BiologicalMyocardial ContractionMyocytes, CardiacReceptor, Cannabinoid, CB1Receptors, Adrenergic, betaSyndrome

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

20462649

Citation

Møller, Søren, and Jens H. Henriksen. "Cirrhotic Cardiomyopathy." Journal of Hepatology, vol. 53, no. 1, 2010, pp. 179-90.
Møller S, Henriksen JH. Cirrhotic cardiomyopathy. J Hepatol. 2010;53(1):179-90.
Møller, S., & Henriksen, J. H. (2010). Cirrhotic cardiomyopathy. Journal of Hepatology, 53(1), 179-90. https://doi.org/10.1016/j.jhep.2010.02.023
Møller S, Henriksen JH. Cirrhotic Cardiomyopathy. J Hepatol. 2010;53(1):179-90. PubMed PMID: 20462649.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cirrhotic cardiomyopathy. AU - Møller,Søren, AU - Henriksen,Jens H, Y1 - 2010/03/31/ PY - 2009/10/22/received PY - 2010/01/26/revised PY - 2010/02/04/accepted PY - 2010/5/14/entrez PY - 2010/5/14/pubmed PY - 2010/9/21/medline SP - 179 EP - 90 JF - Journal of hepatology JO - J Hepatol VL - 53 IS - 1 N2 - Increased cardiac output was first described in patients with cirrhosis more than fifty years ago. Later, various observations have indicated the presence of a latent cardiac dysfunction, which includes a combination of reduced cardiac contractility with systolic and diastolic dysfunction and electrophysiological abnormalities. This syndrome is termed cirrhotic cardiomyopathy. Results of experimental studies indicate the involvement of several mechanisms in the pathophysiology, such as reduced beta-adrenergic receptor signal transduction, altered transmembrane currents and electromechanical coupling, nitric oxide overproduction, and cannabinoid receptor activation. Systolic incompetence in patients can be revealed by pharmacological or physical strain and during stressful procedures, such as transjugular intrahepatic portosystemic shunt insertion and liver transplantation. Systolic dysfunction has recently been implicated in development of renal failure in advanced disease. Diastolic dysfunction reflects delayed left ventricular filling and is partly attributed to ventricular hypertrophy, subendocardial oedema, and altered collagen structure. The QT interval is prolonged in about half of the cirrhotic patients and it may be normalised by beta-blockers. No specific therapy for cirrhotic cardiomyopathy can be recommended, but treatment should be supportive and directed against the cardiac dysfunction. Future research should better describe the prevalence, impact on morbidity and survival, and look for potential treatments. SN - 1600-0641 UR - https://www.unboundmedicine.com/medline/citation/20462649/Cirrhotic_cardiomyopathy_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0168-8278(10)00194-7 DB - PRIME DP - Unbound Medicine ER -