Cardiac sympathetic innervation via middle cervical and stellate ganglia and antiarrhythmic mechanism of bilateral stellectomy

Abstract

Cardiac sympathetic denervation (CSD) is reported to reduce the burden of ventricular tachyarrhythmias [ventricular tachycardia (VT)/ventricular fibrillation (VF)] in cardiomyopathy patients, but the mechanisms behind this benefit are unknown. In addition, the relative contribution to cardiac innervation of the middle cervical ganglion (MCG), which may contain cardiac neurons and is not removed during this procedure, is unclear. The purpose of this study was to compare sympathetic innervation of the heart via the MCG vs. stellate ganglia, assess effects of bilateral CSD on cardiac function and VT/VF, and determine changes in cardiac sympathetic innervation after CSD to elucidate mechanisms of benefit in 6 normal and 18 infarcted pigs. Electrophysiological and hemodynamic parameters were evaluated at baseline, during bilateral stellate stimulation, and during bilateral MCG stimulation in 6 normal and 12 infarcted animals. Bilateral CSD (removal of bilateral stellates and T ganglia) was then performed and MCG stimulation repeated. In addition, in 18 infarcted animals VT/VF inducibility was assessed before and after CSD. In infarcted hearts, MCG stimulation resulted in greater chronotropic and inotropic response than stellate ganglion stimulation. Bilateral CSD acutely reduced VT/VF inducibility by 50% in infarcted hearts and prolonged global activation recovery interval. CSD mitigated effects of MCG stimulation on dispersion of repolarization and T-peak to T-end interval in infarcted hearts, without causing hemodynamic compromise. These data demonstrate that the MCG provides significant cardiac sympathetic innervation before CSD and adequate sympathetic innervation after CSD, maintaining hemodynamic stability. Bilateral CSD reduces VT/VF inducibility by improving electrical stability in infarcted hearts in the setting of sympathetic activation. Sympathetic activation in myocardial infarction leads to arrhythmias and worsens heart failure. Bilateral cardiac sympathetic denervation reduces ventricular tachycardia/ventricular fibrillation inducibility and mitigates effects of sympathetic activation on dispersion of repolarization and T-peak to T-end interval in infarcted hearts. Hemodynamic stability is maintained, as innervation via the middle cervical ganglion is not interrupted.

Efficacy of Stellate Ganglion Blockade in Managing Electrical Storm

“…SGB may also be particularly useful for attenuating burst discharge activity in left stellate ganglion, which has been shown to precede most VT and sudden cardiac death in a canine model of ischemic cardiomyopathy (42–43). Sympathoexcitation increases repolarization heterogeneity (44–46), increases risk of delayed after depolarizations (47,48), and increases arrhythmia inducibility (49). It also modulates peri-infarct tissues harboring circuits capable of facilitating MMVT (50).…”

Antifibrillatory effects of renal denervation on ventricular fibrillation in a canine model of pacing‐induced heart failure

“…Bilateral cardiac sympathetic denervation reduces the VT/VF inducibility and mitigates the effects of sympathetic activation on the dispersion of repolarization in infarcted hearts without causing a haemodynamic compromise (Irie et al . ). These studies may provide mechanistic insight into the beneficial effects of the neural control of the heart in reducing arrhythmias in patients.…”

The autonomic nervous system and ventricular arrhythmias in myocardial infarction and heart failure

“…Notably, sympathetic stimulation increases T‐peak to T‐end interval on the surface ECG, a marker for SCD . Both stellate ganglia provide innervation to the ventricular myocardium …”

“…In the setting of heterogeneity in sympathetic innervation and pathological neural remodeling that accompanies a heterogenous myocardial substrate, effects of sympathetic activation are further amplified leading to greater heterogeneity in action potential durations (APDs) and areas of functional conduction block that promote reentry, Figure …”