Abstracts

Vagal nerve stimulation(VNS) can result in bradycardia experimentally and clinically. VNS therapy has not been shown to cause significant heart rate changes in most cases. Small case series of intraoperative asystole and others of complex changes in heart rate variability with biphasic initial tachycardia followed by bradycardia time locked to VNS stimulation during chronic therapy have also been noted. The objective of this study is to report the characteristics and occurrence of electrophysiologically significant bradycardia noted in three patients during ongoing VNS therapy.
21 patients with medically intractable epilepsy with VNS underwent continuous EKG recording with either Holter Monitoring, VEEG or both. Stimulation on time for VNS was documented by presence of artefact on EKG. Level of VNS stimulation ranged from 0.25 to 2.5 milliamps. Heart rate plots and qualitative changes in cardiac conduction including PR interval and QRS morphology during on and off times of VNS were analyzed . Clinical symptoms suggestive of syncope were asked of patients to try and determine if subjective correlates of cerebral hyoperfusion might be present.
Heart rate recording showed unequivocal changes of bradycardia in three of 21 patients. These decreases in heart rate ranged from 10 to 20 beats per minute from baseline and were time locked to the on times for VNS stimulation. There were no qualitative changes in EKG morphology and all rate changes appeared to be due to sinus bradycardia without nodal block. In the patients with bradycardia, this occurred at stimulation parameters ranging from 1.75 to 2.5 mAmps and reduction of stimulation current produced incremental resolution of bradycardia. Intermittent pallor and weakness suggestive of cerebral hypoperfusion at time of bradycardia was reported in one patient. The two other patients appeared asymptomatic.
Vagal nerve stimulation at high levels may result in bradycardia in some patients. This appears to be mainly asymptomatic and resolves with reduction of VNS stimulation levels. The observed occurrence rates of bradycardia may not be representative of all patients with VNS due to the small numbers screened in this study. The reason for its occurrence is unknown but factors such as anomalies in cardiac vagal innervation or site of VNS stimulator electrode placement may be responsible and warrants further study. The absence of definite adverse hemodynamic events in the patients with significant bradycardia is consistent with lack of significant cardiac side effects seen in most patients with VNS implantation.