During ventricular pacing, LV pump function is maintained best (i.e., at SR level) when pacing at the LV septum or LV apex, potentially because pacing from these sites creates a physiological propagation of electrical conduction.

Optimal pacing in patients with paroxysmal atrial fibrillation/flutter following AV node ablation remains to be determined because VVIR pacing cannot restore AV synchronization and conventional DDD(R) pacing cannot properly cope with atrial tachyarrhythmias. The objective of the present investigation was to study the clinical outcome of 16 of these patients who received a new DDDR pacemaker with an automatic mode switch (Thera DR; Medtronic) immediately after AV node ablation. Arrhythmia-related symptoms before ablation were palpitations in 12, dizziness in 10, exercise intolerance in 8, and syncope in 6 patients. Pacing modes at hospital discharge were DDDR (n = 14) and DDD (n = 2) with an activated mode switch in all patients. After 1 month 12 patients were symptom free. Clinical events occurred in 4 patients (palpitations in 2, dizziness in 1, chest pain in 1, and fatigue in 1), which could be relieved in 3 patients. At discharge as well as at the 1-month follow-up, Holier ECG recorded a total of 12 episodes of atrial fibrillation in 5 patients, which were correctly detected by the pacemaker and followed by mode switching. At the 3-month follow-up (n = 14), 12 patients were symptom free and 2 continued to report symptoms which could not be resolved. All patients remained on an automatic mode switch in either the DDDR (n = 12) or DDD (n = 2) mode. There were no hints of inappropriate mode switching or reports of pacemaker syndrome, and there were no new symptoms related to automatic mode switching. The patients studied were highly symptomatic before implantation due to paroxysmal atrial fibrillation/flutter. After the first follow-up, 81 % of the patients reported no symptoms. Paroxysmal atrial fibrillation/flutter combined with a high-degree AV-block seems no longer to be a contraindication for AV-synchronous pacing.

AVNS is efficient in reducing ventricular rate for at least 3 months using optimized parameters and specifically affects the parasympathetic nerves innervating the AV-node.

INTRODUCTION Drug therapy to reduce the ventricular rate during atrial fibrillation (AF) is effective in only 50% of the patients and limited by side effects. Currently available pacing algorithms are even less effective. The aim of this study was to test the feasibility of chronic AV-Node Inhibition (AVNI) by intra-cardiac parasympathetic nerve stimulation. Our ultimate goal is to develop a pacemaker device with a feature to inhibit AV node function to decrease ventricular rate during AF. METHODS Leads were implanted in the right atrial appendage and right ventricular apex and connected to a pacemaker for AF induction. In addition, an atrial lead (’AVNI lead’) connected to an implantable high frequency neurostimulator was implanted at a site with a strong prolongation of the PQ-time. Immediately after implantation optimal settings, optimal location, acute effects of AVNI on ventricular rate and the possible pro-arrhythmic effects of AVNI were assessed. The ’safety window’ for AVNI was defined as the difference between the output at the AVNI lead that produced atrial capture and the output that produced AVNI. One week after implantation, AF was maintained for one week by burst pacing via the lead in the right atrial appendage. After this 2 week period, the chronic effects of AVNI were assessed weekly for periods ranging from 3 weeks to 7 months. RESULTS In total, 5 goats were studied . The optimal location for AVNI was located at the junction of the coronary sinus and inferior vena cava. Optimal AVNI was found at a stimulation frequency of 30Hz and pulse width of 180 μs in each animal. During the implant procedure “a safety window” appeared to be present. However, it became smaller after a longer period of AVNS. The acute effect of AVNI (averaged over the experiments) was a prolongation of the median R-R interval of 37 % (SD = 21%), which was not significantly different from the chronic effect at the end of the study (average = 32% (SD = 18%). CONCLUSIONS Chronic intra-cardiac AV-node inhibition to reduce the ventricular rate during AF is feasible. Atrial pro-arrhythmic effects can be avoided by optimization of the stimulus parameters and location.