Introduction: Epicardial electrical stimulation of parasympathetic nerves i
nnervating the sinus node has been shown to decrease sinus rate. We investi
gated whether intravascular parasympathetic cardiac nerve stimulation (IPS)
can be achieved over a relatively long-term period to slow the supraventri
cular rate.
Methods and Results: Fifteen dogs were investigated. IFS was performed with
rectangular stimuli (0.05-msec duration, 20 Hz) using a catheter with an e
xpandable electrode basket. The catheter was positioned in the superior ven
a cava (SVC; n = 9) or right pulmonary artery (RPA; n = 6), The basket then
was expanded to hold the catheter in place. Nonfluoroscopic identification
of effective IFS sites was achieved within 5 minutes in the SVC, Increasin
g IFS voltage resulted in a graded response of supraventricular rate slowin
g. A 50% prolongation of the baseline atrial cycle length was achieved with
28 V in the SVC (1,056 +/- 355 msec vs 489 +/- 154 msec; P < 0.001) and 25
V in the RPA (1,181 +/- 306 msec vs 518 +/- 138 msec; P < 0.01), The rate
slowing started immediately after IFS onset, terminated abruptly after IFS
cessation, and could be maintained over 10 hours. A rate slowing effect als
o was observed when the sinus rate was increased by isoproterenol (SVC: 304
+/- 8 msec/RPA: 341 +/- 9 msec with isoproterenol vs SVC: 635 +/- 12 msec
with isoproterenol + LPS at 39 V/ RPA: 584 +/- 16 msec with isoproterenol TPS at 38 V; n = 6).
Conclusion: IFS results in a significant supraventricular rate slowing that
is stable over a relatively long period and may be applied to slow undesir
able sinus tachycardia in acute ischemic syndromes or to counteract undesir
able chronotropic effects of catecholamines during treatment of cardiogenic
or septic shock and acute congestive heart failure.