Document Detail


The Autonomic Nervous System and Heart Failure.
MedLine Citation:
PMID:  24855204     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The pathophysiology of heart failure (HF) is characterized by hemodynamic abnormalities that result in neurohormonal activation and autonomic imbalance with increase in sympathetic activity and withdrawal of vagal activity. Alterations in receptor activation from this autonomic imbalance may have profound effects on cardiac function and structure. Inhibition of the sympathetic drive to the heart through β-receptor blockade has become a standard component of therapy for HF with a dilated left ventricle because of its effectiveness in inhibiting the ventricular structural remodeling process and in prolonging life. Several devices for selective modulation of sympathetic and vagal activity have recently been developed in an attempt to alter the natural history of HF. The optimal counteraction of the excessive sympathetic activity is still unclear. A profound decrease in adrenergic support with excessive blockade of the sympathetic nervous system may result in adverse outcomes in clinical HF. In this review, we analyze the data supporting a contributory role of the autonomic functional alterations on the course of HF, the techniques used to assess autonomic nervous system activity, the evidence for clinical effectiveness of pharmacological and device interventions, and the potential future role of autonomic nervous system modifiers in the management of this syndrome.
Authors:
Viorel G Florea; Jay N Cohn
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Publication Detail:
Type:  REVIEW    
Journal Detail:
Title:  Circulation research     Volume:  114     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2014 May 
Date Detail:
Created Date:  2014-5-23     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  -    
Other Details:
Languages:  ENG     Pagination:  1815-1826     Citation Subset:  -    
Copyright Information:
© 2014 American Heart Association, Inc.
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