alexa Cirrhosis-Associated Cardiomyopathy
ISSN: 2155-6148

Journal of Anesthesia & Clinical Research
Open Access

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Review Article

Cirrhosis-Associated Cardiomyopathy

Ahmed Zaky* and John D Lang

Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA, USA

*Corresponding Author:
Ahmed Zaky, M.D., M.P.H.
Assistant Professor of Anesthesiology and Pain Medicine
VA Puget Sound Hospital/University of Washington
1660 S Columbian way, Seattle
WA 98108, S-112-ANES, USA
Tel: 206 277 6723
Fax: 206 764 2914
E-mail: [email protected]

Received Date: December 04, 2012; Accepted Date: December 21, 2012; Published Date: December 25, 2012

Citation: Zaky A, Lang JD (2012) Cirrhosis-Associated Cardiomyopathy. J Anesth Clin Res 3:266. doi: 10.4172/2155-6148.1000266

Copyright: © 2012 Zaky A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Liver cirrhosis is the 12th leading cause of death in the US. The heart is one of the most adversely affected organs in liver cirrhosis. Cirrhosis-induced cardiomyopathy describes the cardiac dysfunction in patients with cirrhosis characterized by impaired contractile response to stress and/or altered diastolic relaxation with electrophysiologic abnormalities in the absence of other known cardiac disease. The current definition of cirrhosis-induced cardiomyopathy does not take into account recent evidence of resting contractile and relaxation dysfunction that can be appreciated by advanced imaging tools such as Doppler tissue imaging and cardiac magnetic resonance imaging. Cirrhosis-induced cardiomyopathy is caused by cellular as well as physiological mechanisms including but not limited to: beta adrenergic receptor dysfunction, calcium channelopathy, elevated levels of catecholamines, elevated levels of nitric oxide, carbon monoxide and hydrogen sulphide and stimulation of endogenous cannabinoid pathways capable of producing negative inotropic, relaxation, and electrophysiological defects. Currently there is no specific therapy for cirrhosis-induced cardiomyopathy.

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