Document Detail


Venous congestion and endothelial cell activation in acute decompensated heart failure.
MedLine Citation:
PMID:  20424989     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Despite accumulating clinical evidence supporting a key role for venous congestion in the development of acute decompensated heart failure (ADHF), there remain several gaps in our knowledge of the pathophysiology of ADHF. Specifically, the biomechanically driven effects of venous congestion on the vascular endothelium (the largest endocrine/paracrine organ of the body), on neurohormonal activation, and on renal and cardiac dysfunction remain largely unexplored. We propose that venous congestion is a fundamental, hemodynamic stimulus for vascular inflammation, which plays a key role in the development and possibly the resolution of ADHF through vascular, humoral, renal, and cardiac mechanisms. A better understanding of the role of venous congestion and endothelial activation in the pathophysiology of ADHF may provide a strong rationale for near-future testing of treatment strategies that target biomechanically driven inflammation. Targeting vascular and systemic inflammation before symptoms arise may prevent progression to overt clinical decompensation in the ADHF syndrome.
Authors:
Anjali Ganda; Duygu Onat; Ryan T Demmer; Elaine Wan; Timothy J Vittorio; Hani N Sabbah; Paolo C Colombo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Current heart failure reports     Volume:  7     ISSN:  1546-9549     ISO Abbreviation:  Curr Heart Fail Rep     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-25     Completed Date:  2010-10-01     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101196487     Medline TA:  Curr Heart Fail Rep     Country:  United States    
Other Details:
Languages:  eng     Pagination:  66-74     Citation Subset:  IM    
Affiliation:
Division of Nephrology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. ag355@columbia.edu
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MeSH Terms
Descriptor/Qualifier:
Endothelial Cells / metabolism*
Heart Failure / complications*,  physiopathology*
Humans
Hyperemia / etiology*
Severity of Illness Index

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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