Department of Engineering Mathematics and Internetworking, Dalhousie University, Nova Scotia, Canada
Joseph Hadaya
UCLA Cardiac Arrhythmia Center and UCLA Neurocardiology Research Program of Excellence, Los Angeles, United States; UCLA Molecular, Cellular, and Integrative Physiology Program, Los Angeles, United States
Alex Karavos
Department of Engineering Mathematics and Internetworking, Dalhousie University, Nova Scotia, Canada
Taro Temma
UCLA Cardiac Arrhythmia Center and UCLA Neurocardiology Research Program of Excellence, Los Angeles, United States
Yuichi Hori
UCLA Cardiac Arrhythmia Center and UCLA Neurocardiology Research Program of Excellence, Los Angeles, United States
J Andrew Armour
UCLA Cardiac Arrhythmia Center and UCLA Neurocardiology Research Program of Excellence, Los Angeles, United States
Guy Kember
Department of Engineering Mathematics and Internetworking, Dalhousie University, Nova Scotia, Canada
UCLA Cardiac Arrhythmia Center and UCLA Neurocardiology Research Program of Excellence, Los Angeles, United States; UCLA Molecular, Cellular, and Integrative Physiology Program, Los Angeles, United States
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 (HF). 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 HF. Future therapies that target the SG 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 HF and control subjects during extended in-vivo extracellular microelectrode recordings. We find that information processing and cardiac control in chronic HF 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.