Key result
This review summarizes current knowledge of carotid body chemoreflex function in experimental models of chronic heart failure and its potential translation to human treatment.
Why the study?
Does modulation or ablation of carotid body chemoreceptors improve autonomic function, breathing control, and survival in chronic heart failure?
Does modulation or ablation of carotid body chemoreceptors improve autonomic function, breathing control, and survival in chronic heart failure?
The carotid body chemoreflex plays a critical role in the progression of heart failure, and its modulation represents a potential therapeutic target for improving autonomic function and survival.
Carotid body modulation merits human trials in heart failure; extends experimental models but leaves clinical efficacy open.
Chronic heart failure (CHF) is a global health problem affecting millions of people. Autonomic dysfunction and disordered breathing patterns are commonly observed in patients with CHF, and both are strongly related to poor prognosis and high mortality risk. Tonic activation of carotid body (CB) chemoreceptors contributes to sympathoexcitation and disordered breathing patterns in experimental models of CHF. Recent studies show that ablation of the CB chemoreceptors improves autonomic function and breathing control in CHF and improves survival. These exciting findings indicate that alterations in CB function are critical to the progression of CHF. Therefore, better understanding of the physiology of the CB chemoreflex in CHF could lead to improvements in current treatments and clinical management of patients with CHF characterized by high chemosensitivity. Accordingly, the main focus of this brief review is to summarize current knowledge of CB chemoreflex function in different experimental models of CHF and to comment on their potential translation to treatment of human CHF.
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Andrade et al. (2015) conducted a review in Chronic heart failure (CHF). Carotid body chemoreceptor ablation was evaluated. This review summarizes current knowledge of carotid body chemoreflex function in experimental models of chronic heart failure and its potential translation to human treatment.
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