Experimental Model of Focal Atrial Tachycardia: Clinical Correlates. (26th April 2013)

• Record Type: Journal Article
• Authors: LIU, YU; SCHERLAG, BENJAMIN J.; FAN, YOUQI; MAO, JUN; HEPLER, ERIC; VARMA, VANDANA; MALE, SHAILESH; XIA, WENFANG; HUANG, HE; PO, SUNNY S.
• Is Part Of: Journal of cardiovascular electrophysiology. Volume 24:Number 8(2013:Aug.)
• Page Start: 909
• Page End: 913
• Publication Date: 2013-04-26
• Subjects: autonomic nervous system -- focal atrial tachycardia -- noncontact mapping; Blood vessels -- Physiology -- Periodicals; Electrophysiology -- Periodicals; Heart -- Physiology -- Periodicals; 612.1
• DOI: 10.1111/jce.12160
• Languages: English
• ISSNs: 1045-3873

Abstract

Focal Atrial Tachycardia Model: Background: The mechanisms underlying focal atrial tachycardia (AT) are unclear. Methods: In 14 pentobarbital anesthetized dogs, a right thoracotomy allowed electrical stimulation (ES) of the anterior right ganglionated plexi (ARGP). After ES was applied to the ARGP at baseline, atropine, 1 mg/cc, was injected into the ARGP and repeat stimulation applied. After a left thoracotomy (n = 8), a similar procedure was followed by atropine injected into the superior left (SL) GP. Results: ES (0.6–3.2 V) applied to the ARGP and SLGP caused an average reduction in sinus rate from 151 ± 14/min to 60 ± 11/min. At ≥4.5 V atrial fibrillation (AF) was induced (duration 48 ± 14 seconds). After injection of atropine into the ARGP or SLGP, ES applied to these GP induced no slowing of the sinus rate. Runs of AT were induced at an average voltage of 10 ± 2 V in 14 experiments (duration ≥4 minutes). AT was localized by ice mapping or by 3D noncontact mapping to the crista terminalis (n = 6), AV junction (n = 2) or a focal site at the left superior pulmonary vein (6). In AT lasting <4 minutes (n = 2), epinephrine injected into the GP significantly increased the AT duration. In 4/4 experiments, sustained AT could be terminated by intravenous esmolol. Conclusions: Atropine injected into the ARGP or SLGP promotes ES‐induced AT whose duration is increased by adrenergic agonists and terminated by beta blockade. Presumably cholinergic blockade and accentuated release of adrenergic neurotransmitters provide the AT mechanism. The induced AT was found to be localized at sites similar to those reported clinically.