TY - JOUR
T1 - Increased vagal cardiac nerve traffic prolongs ventricular refractoriness in patients undergoing electrophysiology testing
AU - Ellenbogen, Kenneth A.
AU - Smith, Michael L.
AU - Eckberg, Dwain L.
PY - 1990/6/1
Y1 - 1990/6/1
N2 - Stimulation of the vagus nerve in animals causes prolongation of sinus cycle length, abioventricular nodal conduction and ventricular refractoriness. Vagal stimulation appears to have a protective effect in animal models of sudden death. The electrophysiologic effects of enhanced vagal activity on right ventricular (RV) refractoriness in man have not been studied previously. The comparative effects of enhanced vagal tone (neck suction to -60 mm Hg) on sinus cycle length and RV refractoriness were assessed in 26 patients. The electrophysiologic effects of vagal activation by stimulation of carotid baroreceptors with neck suction were compared to the effect of carotid and aortic baroreceptor stimulation with phenylephrine infusion in 12 patients. During neck suction, mean sinus cycle length (819 ± 32 ms) was prolonged by 146 ± 20 ms (p < 0.0001). The mean RV effective refractory period (ERP) and functional refractory period (FRP) were prolonged by 4 ± 1 ms and 5 ± 1 ms (p = 0.0001 and 0.0002, respectively). The mean change in RV ERP and FRP correlated with the peak change in sinus cycle length during neck suction (r = 0.46 and r = 0.58, respectively). intravenous phenyl phrine infusion, the mean change in RV ERP and FRP was S ± 2 ms (p < 0.04) and 10 ± 3 ms (p < 0.01), respectively. These results show that reflex vagal stimulation with neck suction or phenylephrine infusion causes a small but significant prolongation in RV refractoriness. These findings imply that the potential benefits of enhanced vagal tone in preventing sudden death may be indirectly mediated by changes in ventricular refractoriness.
AB - Stimulation of the vagus nerve in animals causes prolongation of sinus cycle length, abioventricular nodal conduction and ventricular refractoriness. Vagal stimulation appears to have a protective effect in animal models of sudden death. The electrophysiologic effects of enhanced vagal activity on right ventricular (RV) refractoriness in man have not been studied previously. The comparative effects of enhanced vagal tone (neck suction to -60 mm Hg) on sinus cycle length and RV refractoriness were assessed in 26 patients. The electrophysiologic effects of vagal activation by stimulation of carotid baroreceptors with neck suction were compared to the effect of carotid and aortic baroreceptor stimulation with phenylephrine infusion in 12 patients. During neck suction, mean sinus cycle length (819 ± 32 ms) was prolonged by 146 ± 20 ms (p < 0.0001). The mean RV effective refractory period (ERP) and functional refractory period (FRP) were prolonged by 4 ± 1 ms and 5 ± 1 ms (p = 0.0001 and 0.0002, respectively). The mean change in RV ERP and FRP correlated with the peak change in sinus cycle length during neck suction (r = 0.46 and r = 0.58, respectively). intravenous phenyl phrine infusion, the mean change in RV ERP and FRP was S ± 2 ms (p < 0.04) and 10 ± 3 ms (p < 0.01), respectively. These results show that reflex vagal stimulation with neck suction or phenylephrine infusion causes a small but significant prolongation in RV refractoriness. These findings imply that the potential benefits of enhanced vagal tone in preventing sudden death may be indirectly mediated by changes in ventricular refractoriness.
UR - http://www.scopus.com/inward/record.url?scp=0025331904&partnerID=8YFLogxK
U2 - 10.1016/0002-9149(90)91325-Z
DO - 10.1016/0002-9149(90)91325-Z
M3 - Article
C2 - 2343822
AN - SCOPUS:0025331904
SN - 0002-9149
VL - 65
SP - 1345
EP - 1350
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 20
ER -