Cardioinhibition Secondary to Ventricular Pacing

Abstract

A 19-year-old woman with exercise-induced palpitations and recurrent syncopal episodes was referred for electrophysiologic study. Holter monitoring showed sinus arrhythmia, first-degree atrioventricular (AV) block (PR interval: 280 msec), and occasional type I, 2 • degree AV block. The Jorge Salinas received a grant from the Fundación Carolina, Spain, for participating in a training program in cardiac electrophysiology in the Cardiovascular Institute, Figure 1. Upper panel: Sinus node inhibition during ventricular pacing in the absence of VA conduction. At the end of pacing, there is suprahisian AV block of one atrial beat (asterisk), which can be better appreciated at the bottom panel. This observation was reproducible and indicates that cardioinhibitory effects of ventricular pacing were also elicited on the AV node. A = atrial beat; P = ventricular paced beat.electrophysiologic study showed normal corrected sinus node recovery time (350 msec), normal sinoatrial conduction time (105 msec), and dual antegrade nodal pathways. The AV node Wenckebach block cycle length was 380 msec. There was neither inducible tachycardia nor VA conduction. Surprisingly, a sustained sinus node inhibition was observed during ventricular pacing at 600 msec cycle length. Suprahisian AV block was also observed once ventricular pacing was stopped (Fig. 1). What is the mechanism responsible for this phenomenon? DiscussionSinus node inhibition during ventricular pacing in the absence of VA conduction is rarely observed during electrophysiologic studies. 1,2 Hypothetically, it is caused by an increase in vagal activity secondary to stimulation of ventricular mechanoreceptors. 3 To verify this hypothesis, we assessed

Premature atrial complexes and atrial couplets: What is the mechanism?

“…The observations that atrial ectopy was recorded during ventricular pacing only when a sinus beat conducted anterogradely through the AV node (Figure 2B), and those atrial couplets were temporarily suppressed with mechanical trauma in the region of the compact AV node (Figure 1B), argue that anterograde AV nodal conduction is necessary for the development of PACs. While cardioinhibition involving a vagal mechanism has been described during ventricular pacing, 1 this mechanism seems unlikely as sinus rate did not change significantly during ventricular pacing. The retrograde limb responsible for atrial ectopy appears less straightforward.…”