Background
Intra-myocardial nerve sprouting after myocardial infarction is associated with ventricular arrhythmias (VAs). Whether human stellate ganglia remodel in association with cardiac pathology is unknown. The purpose of this study was to determine whether cardiac pathology is associated with remodeling of the stellate ganglia in humans.
Methods and Results
Left stellate ganglia (LSG) were collected from patients undergoing sympathetic denervation for intractable ventricular arrhythmias, and from cadavers, along with intact hearts. Clinical data on patients and cadaveric subjects were reviewed. We classified ganglia from normal; scarred; and non-ischemic cardiomyopathic hearts without scar as NL (n=3); SCAR (n=24); and NICM (n=7), respectively. Within LSG, neuronal size, density, fibrosis, synaptic density and nerve sprouting were determined. Nerve density and sprouting were also quantified in cadaveric hearts. Mean neuronal size in NL, SCAR, and NICM groups were; 320±4μm2, 372±10μm2,and 435±10μm2 (p=0.002). No significant differences in neuronal density and fibrosis were present between the groups. Synaptic density in SCAR and NICMganglia were 57.8±11.2um2/ mm2 (p=0.039) and 44.5±7.9um2/ mm2 (p=0.084) respectively, compared to the NL, 17.8±7um2/ mm2 (overall p=0.162). There were no significant differences in LSG nerve sprouting or myocardial nerve density between the groups.
Conclusions
Neuronal hypertrophy withinLSGis associated with chronic cardiomyopathy in humans. Ganglionic and myocardial nerve sprouting and nerve density were not significantly different. These changes may be related to increased cardiac sympathetic signaling and VAs. Further studies are needed to determine the electrophysiologic consequences of extra-cardiac neuronal remodeling in humans.