Inducibility of Atrial and Ventricular Arrhythmias Along the Ligament of Marshall: Role of Autonomic Factors

Background: The mechanism(s) underlying atrial fibrillation (AF) initiation along the ligament of Marshall (LOM) remains controversial. Objectives: We sought to examine the role of the autonomic nervous system in arrhythmogenesis along the LOM. Methods: In 31 anesthetized dogs, a left thoracotomy exposed the LOM. During atrial pacing, high‐frequency stimulation (HFS: 200 Hz, 0.1 ms pulse width, 40 ms duration, 0.6–12 V) was delivered during atrial refractoriness to different sites of LOM (LOM CS = near coronary sinus; LOM LIPV = near left inferior pulmonary vein; LOM LS‐LIPV = between LIPV and left superior pulmonary vein (LSPV); LOM LSPV = near LSPV). HFS was repeated after intravenous administration of esmolol (1 mg/kg; n = 9) or atropine (2 mg; n = 12). Norepinephrine (10 −7 M, 0.4 cc) was injected into LOM LSPV (n = 5). Results: The median voltages for HFS to induce AF were 3.2 V, 3.2 V, 8.0 V* ,‡ , and 12 V* ,‡ at LOM CS , LOM LIPV , LOM LS‐LIPV , and LOM LSPV , respectively (*P < 0.01, compared with LOM CS and ‡ P < 0.01, compared with LOM LIPV ). Esmolol or atropine markedly increased the threshold for AF induction. Ventricular tachycardias (VT) and accelerated junctional rhythm were induced in 8 of 12 and 6 of 12 dogs after atropine administration, respectively. Sustained VT occurred within minutes in 5 of 5 dogs receiving norepinephrine injection into the LOM LSPV. Conclusion: HFS induced AF along LOM with a gradient of stimulation thresholds from LOM CS (lowest) toward LOM LSPV (highest). This response was inhibited by esmolol or atropine. These data suggest an autonomic basis for AF initiation in LOM, and both sympathetic and parasympathetic neural elements play an important role in AF initiation. Hyperactivity of the sympathetic neural elements in LOM may be crucial in the initiation of ventricular tachyarrhythmias.