Anatomy and physiology of the right interganglionic nerve: implications for the pathophysiology of inappropriate sinus tachycardia

Abstract

Objective: To simulate inappropriate sinus tachycardia (IST) in experimental animals.

Background: We recently found that epinephrine injected into the anterior right ganglionated plexi (ARGP) adjacent to the sinoatrial (SA) node induced an arrhythmia simulating IST.

Methods: In 19 anesthetized dogs, via a right thoracotomy, the course of the interganglionic nerve (IGN) from the right stellate ganglion along the superior vena cava to the heart was delineated. High-frequency stimulation (HFS; 0.1 msec duration, 20 Hz, 4.5-9.3 V) was applied to IGN at the junction of innominate vein and SVC.

Results: HFS of the IGN significantly increased the sinus rate (SR) (baseline: 156 +/- 19 beats/minutes [bpm], 4.5 V: 191 +/- 28 bpm*, 8.0 V: 207 +/- 23 bpm*, 9.3 V: 216 +/- 18 bpm*; *P < 0.01 compared to baseline) without significant changes in A-H interval or blood pressure. P-wave morphology, ice mapping, and noncontact mapping indicated that this tachycardia was sinus tachycardia. In 8 of 19 dogs, injecting hexamethonium (5 mg), a ganglionic blocker, into the ARGP attenuated the response elicited by IGN stimulation (baseline: 160 +/- 21 bpm, 4.5 V: 172 +/- 32 bpm, 8.0 V: 197 +/- 32 bpm*, 9.3 V: 206 +/- 26 bpm*; *P < 0.05 compared to baseline). In 19 of 19 animals, after formaldehyde injection into the ARGP, SR acceleration induced by IGN stimulation was markedly attenuated (baseline: 149 +/- 17 bpm, 4.5 V: 151 +/- 21 bpm, 8.0 V: 155 +/- 23 bpm, 9.3 V: 167 +/- 24 bpm*; *P < 0.05 compared to baseline).

Conclusions: HFS of the IGN caused a selective and significant acceleration of the SR. A significant portion of IGN traverses the ARGP or synapses with the autonomic ganglia in the ARGP before en route to the SA node. Dysautonomia involving the IGN and/or ARGP may play an important role in IST.