Document Detail

Selective carotid body ablation in experimental heart failure: a new therapeutic tool to improve cardiorespiratory control.
MedLine Citation:
PMID:  25398714     Owner:  NLM     Status:  Publisher    
Chronic heart failure (CHF) is a leading medical problem worldwide. Common hallmarks of CHF include autonomic imbalance and breathing disorders, both of which are closely related to the progression of the disease and strongly predict mortality in CHF patients. The role played by the carotid body (CB) chemoreceptors on the progression of CHF has received attention since enhanced carotid chemoreflex drive is thought to contribute to autonomic dysfunction, abnormal breathing patterns, and increased mortality in CHF. Therefore, therapeutic tools intended to normalize CB-mediated chemoreflex drive could have the potential to better improve life quality and decrease mortality of CHF patients. In experimental CHF it has been shown an enhancement of the CB chemoreflex drive, elevated sympathetic outflow, increased resting breathing variability and apnoea incidence, and desensitization of the baroreflex. Notably, selective elimination of the CB reduced central presympathetic neuronal activation, normalized sympathetic outflow and baroreflex sensitivity, and stabilized breathing function in CHF. More remarkably, CB ablation has been shown to be a valuable therapeutic tool that significantly reduced aberrant cardiac remodeling and improved left ventricle ejection fraction and reduced cardiac arrhythmogenesis. Most importantly, CHF animals that underwent CB ablation showed a marked improvement in survival rate. Interestingly, a case report from a heart failure patient in which unilateral CB ablation was performed showed promising results with significant improvement in autonomic balance and breathing variability. Together, CHF data from experimental animals as well as humans unveil a major role for the carotid body chemoreceptors in the progression of heart failure and support the notion that CB ablation could represent a novel therapeutic strategy to reduce cardiorespiratory dysfunction and improve survival during heart failure. This article is protected by copyright. All rights reserved.
Rodrigo Del Rio; David C Andrade; Noah J Marcus; Harold D Schultz
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-11-13
Journal Detail:
Title:  Experimental physiology     Volume:  -     ISSN:  1469-445X     ISO Abbreviation:  Exp. Physiol.     Publication Date:  2014 Nov 
Date Detail:
Created Date:  2014-11-15     Completed Date:  -     Revised Date:  2014-11-16    
Medline Journal Info:
Nlm Unique ID:  9002940     Medline TA:  Exp Physiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
This article is protected by copyright. All rights reserved.
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