Key result
Pacing-induced heart failure in a porcine model was associated with significantly higher rates of high neural cofluctuations in the stellate ganglion compared to healthy controls (d = 1.59, p = 0.011).
Why the study?
Future heart failure therapies targeting the stellate ganglion require understanding its interneuronal networking capabilities and cardiopulmonary transduction processing to modify pathological remodeling.
Does chronic pacing-induced heart failure alter stellate ganglion neural network processing and cardiac control linkage in a porcine model?
Does chronic pacing-induced heart failure alter stellate ganglion neural network processing and cardiac control linkage in a porcine model?
Standardized Mean Difference: 1.59
p-value: p=0.011
Disrupted stellate ganglion dynamics in experimental HF; leaves open whether targeting these networks improves human outcomes.
Stellate ganglia within the intrathoracic cardiac control system receive and integrate central, peripheral, and cardiopulmonary information to produce postganglionic cardiac sympathetic inputs. Pathological anatomical and structural remodeling occurs within the neurons of the stellate ganglion (SG) in the setting of heart failure. A large proportion of SG neurons function as interneurons whose networking capabilities are largely unknown. Current therapies are limited to targeting sympathetic activity at the cardiac level or surgical interventions such as stellectomy, to treat heart failure. Future therapies that target the stellate ganglion will require understanding of their networking capabilities to modify any pathological remodeling. We observe SG networking by examining cofluctuation and specificity of SG networked activity to cardiac cycle phases. We investigate network processing of cardiopulmonary transduction by SG neuronal populations in porcine with chronic pacing-induced heart failure and control subjects during extended in-vivo extracellular microelectrode recordings. We find that information processing and cardiac control in chronic heart failure by the SG, relative to controls, exhibits: i) more frequent, short-lived, high magnitude cofluctuations, ii) greater variation in neural specificity to cardiac cycles, and iii) neural network activity and cardiac control linkage that depends on disease state and cofluctuation magnitude.
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Gurel et al. (2021) studied Heart failure (n=17). Pacing-induced heart failure vs. Healthy controls was evaluated on Mean event rate of high cofluctuations (ER_MEAN) (d = 1.59, p=0.011). Pacing-induced heart failure in a porcine model was associated with significantly higher rates of high neural cofluctuations in the stellate ganglion compared to healthy controls (d = 1.59, p = 0.011).
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