Anatomy and Physiology of the Right Interganglionic Nerve: Implications for the Pathophysiology of Inappropriate Sinus Tachycardia

Abstract

To simulate inappropriate sinus tachycardia (IST) in experimental animals. We recently found that epinephrine injected into the anterior right ganglionated plexi (ARGP) adjacent to the sinoatrial (SA) node induced an arrhythmia simulating IST. 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. 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). 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.