New Treatments for Vasovagal Syncope May 16, 2011Posted by Peng-Sheng Chen, MD, FHRS in Science & Research, Scientific Sessions.
Tags: Heart Rhythm 2011
Many interesting basic-translational science abstracts were presented during the Heart Rhythm Society’s 32nd Annual Scientific Sessions. The following two abstracts provide new hope for breakthrough treatment of the vasovagal syncope (VVS), a major clinical problem for EP consultants.
Vagal Nerve Stimulation for the Treatment of Vasovagal Syncope
Appropriately delivered electrical impulses to the cervical vagus nerve could theoretically interrupt the heart rate (HR) and vasoactive effects of vasovagal syncope. Mickelsen et al (PO2-123) investigated direct current nerve block/inhibition (DCI) techniques to temporarily and reversibly interrupt the afferent and efferent vagus nerve signals involved in neurocardiogenic syncope. Left and right vagal nerves were stimulated (VNS) in anesthetized dogs (n=10). VNS of left or right vagus reduced HR by 57-71% in all animals. Delivery of DCI (2.2-4.6V) to the downstream electrode pair restored HR to baseline within 2 seconds. This effect was sustained over the duration of the stimulus. BP dropped substantially with VNS-induced bradycardia; BP returned to baseline with DCI despite continued upstream excess VNS. Afferent VNS produced an on average 17% decrease in BP. Hypotension with excess afferent VNS occurred even when the heart rate was maintained by pacing. This afferent BP effect was also blocked with DCI. The authors conclude that it is feasible to interrupt both efferent and afferent vagus nerve signals with DCI, ameliorating cardiovascular vagal effects. Unlike pacemaker therapy this model suggests that DCI may also interrupt vasodepressor reflexes associated with hypotension.
GP Ablation for the Treatment of vasovagal syncope
Shi et al (PO3-162) evaluated whether vasovagal syncope (VVS) could be prevented by selective endocardial vagal denervation. The authors studied 8 patients with a mean age 52 years. All of the patients (3 men and 5 women) suffered from recurrent episodes of VVS. Head-up tilt testing was positive in all patients. Ganglionated plexi (GP) was located by high-frequency stimulation in left atrium. A positive vagal response was defined as transient ventricular asystole, atrioventricular (AV) block, or an increase in RR interval by 50%. The RF energy was applied at left superior GP and in 8 patients, right superior GP in 3 patients, left lateral GP in 2 patients using an 8mm tip catheter (60W, 60oC). Vagal response was observed during ablation in all patients. The end point of procedure was ablation at least 60 seconds until inhibition of the vagal response at each target. After a follow-up of 24 ± 16 (6 – 45) months, 4 of the 8 patients reported prodromes but none had recurrence of episodes of vasovagal syncope. All patients reported significant improvement in quality of life after denervation. No complications occurred. The authors conclude that intensive catheter ablation of Ganglionated plexi in left atrium may prevent vasovagal syncope in patients in a relative long term follow-up.