Key result
Central chemoreflex activation may drive disordered breathing and autonomic dysfunction in HFpEF.
Why the study?
While peripheral chemoreflex drive is established in HFrEF, less is known about the neural mechanisms mediating cardio-respiratory disturbances in HFpEF.
Understanding the role of the central chemoreflex and retrotrapezoid nucleus in HFpEF pathophysiology may guide the development of novel interventions for cardio-respiratory outcomes.
A strong association between chemoreflex hypersensitivity, disordered breathing, and elevated sympathetic activity has been shown in experimental and human heart failure (HF). The contribution of chemoreflex hypersensitivity in HF pathophysiology is incompletely understood. There is ample evidence that increased peripheral chemoreflex drive in HF with reduced ejection fraction (HFrEF; EF<40%) leads to pathophysiological changes in autonomic and cardio-respiratory control, but less is known about the neural mechanisms mediating cardio-respiratory disturbances in HF with preserved EF (HFpEF; EF>50%). Importantly, it has been shown that activation of the central chemoreflex worsens autonomic dysfunction in experimental HFpEF, an effect mediated in part by the activation of C1 catecholaminergic neurons neighboring the retrotrapezoid nucleus (RTN), an important region for central chemoreflex control of respiratory and autonomic function. Accordingly, the main purpose of this brief review is to discuss the possible role played by activation of central chemoreflex pathways on autonomic function and its potential role in precipitating disordered breathing in HFpEF. Improving understanding of the contribution of the central chemoreflex to the pathophysiology of HFpEF may help in development of novel interventions intended to improve cardio-respiratory outcomes in HFpEF.
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Toledo et al. (2022) conducted a review in Heart Failure with Preserved Ejection Fraction (HFpEF). Activation of central chemoreflex pathways, particularly involving the retrotrapezoid nucleus, may play a fundamental role in precipitating disordered breathing and autonomic dysfunction in HFpEF.
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