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*(,double dagger), and 12 V*(,double dagger) at LOM(CS), LOM(LIPV), LOM(LS-LIPV), and LOM(LSPV), respectively (*P < 0.01, compared with LOM(CS) and double dagger 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.