Electroanatomic Remodeling of the Left Stellate Ganglion After Myocardial Infarction

Abstract

Objectives The purpose of this study was to evaluate the changes of left stellate ganglionic nerve activity (SGNA) and left thoracic vagal nerve activity (VNA) after acute myocardial infarction (MI). Background Whether MI results in remodeling of extracardiac nerve activity remains unclear. Methods We implanted radiotransmitters to record the SGNA, VNA, and electrocardiogram in 9 ambulatory dogs. After baseline monitoring, MI was created by 1-h balloon occlusion of the coronary arteries. The dogs were then continuously monitored for 2 months. Both stellate ganglia were stained for growth-associated protein 43 and synaptophysin. The stellate ganglia from 5 normal dogs were used as control. Results MI increased 24-h integrated SGNA from 7.44 ± 7.19 Ln(Vs)/day at baseline to 8.09 ± 7.75 Ln(Vs)/day after the MI (p < 0.05). The 24-h integrated VNA before and after the MI was 5.29 ± 5.04 Ln(Vs)/day and 5.58 ± 5.15 Ln(Vs)/day, respectively (p < 0.05). A significant 24-h circadian variation was noted for the SGNA (p < 0.05) but not the VNA. The SGNA/VNA ratio also showed significant circadian variation. The nerve densities from the left SG were 63,218 ± 34,719 μm2/mm2 and 20,623 ± 4,926 μm2/mm2 for growth-associated protein 43 (p < 0.05) and were 32,116 ± 8,190 μm2/mm2 and 16,326 ± 4,679 μm2/mm2 for synaptophysin (p < 0.05) in MI and control groups, respectively. The right SG also showed increased nerve density after MI (p < 0.05). Conclusions MI results in persistent increase in the synaptic density of bilateral stellate ganglia and is associated with increased SGNA and VNA. There is a circadian variation of the SGNA/VNA ratio. These data indicate significant remodeling of the extracardiac autonomic nerve activity and structures after MI.

Focal myocardial infarction induces global remodeling of cardiac sympathetic innervation: neural remodeling in a spatial context

“…Heterogeneous postinfarct sprouting of sympathetic nerves has been reported in humans and animals (12,26,29,30). Neurotrophins released at the infarct site are trafficked to stellate ganglia (29) and presumably the intrinsic cardiac network (ICN), where they induce neuronal remodeling (2,4,9), increase stellate ganglion nerve activity (9), and cause sprouting of sympathetic nerves in the heart. The porcine model of patchy myocardial scars showed nerve sprouting and increased nerve density at scar-border zone regions consistent with previous findings (13,21).…”

Dissociation of hemodynamic and electrocardiographic indexes of myocardial ischemia in pigs with hibernating myocardium and sudden cardiac death

“…We used heart rate and systolic blood pressure as surrogates of generalized sympathetic activity. Nevertheless, these are indirect hemodynamic indexes that reflect global sympathetic activation, and they may not always correlate with alterations in myocardial sympathetic nerve activity, which have been measured using in vivo recordings in dogs (12,31). The latter studies demonstrate that increased sympathetic nerve activity precedes the development of ventricular arrhythmias and displays a diurnal variation resulting in myocardial sympathovagal imbalance that is maximal in the morning (8 AM to 12 PM) and correlates with the time frame during which spontaneous VT/VF developed in our swine model.…”

Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias

“…Follow-up studies demonstrated that myocardial infarction causes the upregulation of proteins that contributed to nerve growth (nerve growth factor, growth-associated protein 43, and synaptophysin) in both the infarcted site 72 and the more upstream bilateral stellate ganglia. 73 Interestingly, sympathetic nerve sprouting itself can lead to an increased incidence of VF without concomitant cardiac ischemia. It was found that rabbits given a high-cholesterol diet developed myocardial hypertrophy and cardiac sympathetic hyperinnervation without coronary artery disease along with an increased vulnerability to VF.…”

“…Although increased stellate ganglion nerve activity contributes to VF and SCD in myocardial infarction, acute myocardial infarction itself can cause an increase in nerve activity and nerve density of the LSG-electroanatomic remodeling. 73 This generates a vicious cycle that can lead to more ischemia, VF, and SCD.…”