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Dual effects of concealed A-V nodal conduction in man
Insights
Interpolated premature ventricular contractions (PVCs) can alter A-V nodal conduction. This study found that PVCs can reduce the functional refractory period of the A-V node, impacting subsequent atrial stimuli.
Area of Science:
- Electrophysiology
- Cardiology
- Cardiac Electrophysiology
Background:
- Premature ventricular contractions (PVCs) can affect atrioventricular (A-V) nodal conduction.
- The impact of partially depressed A-V nodal conduction following a PVC on subsequent premature atrial stimuli remains unclear.
Observation:
- Three patients were studied to assess the effect of interpolated PVCs on the A-V node's functional refractory period.
- Measurements were taken using programmed atrial and ventricular stimuli.
Findings:
- Interpolated PVCs depressed A-V nodal conduction in the subsequent sinus beat (prolonging the A-H interval).
- Subsequent premature atrial stimuli showed relative facilitation of A-V nodal conduction.
- The apparent functional refractory period of the A-V node was reduced compared to baseline or when using only atrial extrastimulus techniques.
Implications:
- Interpolated PVCs have a dual effect: depressing subsequent sinus impulse conduction while facilitating premature atrial impulse conduction.
- This finding refines our understanding of A-V nodal refractoriness in the context of ventricular ectopy.
- Further research may explore clinical consequences of this altered refractoriness.
Abstract:
An interpolated premature ventricular contraction (PVC) may produce either complete block of the next sinus impulse or depression of A-V nodal conduction with a prolonged A-H interval. When a PVC results in partial depression of a A-V nodal conduction, the effect on subsequent premature atrial stimuli is unknown. The authors have recently observed three patients in which the effect of a premature ventricular stimulus with interpolation on the functional refractory period of the A-V node could be measured. In case one an interpolated PVC sufficient to prolong the A-H interval from 80 to 120 msec was followed by programmed premature atrial stimuli which resulted in no additional A-V nodal delay, and the apparent functional refractory period of the A-V node was reduced from 420 to 330 msec when compared with the atrial extrastimulus technique. In case two a programmed ventricular extrastimulus prolonged the A-H interval in the following sinus beat from 120 to 240 msec; atrial extrastimuli then resulted in only minimal increments in A-V nodal delay and the apparent functional refractory period of the A-V node was reduced from 590 msec. A ventricular extrastimulus in case three increased the resting A-H interval from 60 to 115 msec; conduction of atrial extrastimuli then resulted in a reduction in the functional refractory period of the A-V node from 465 to 400 msec. In each case an interpolated premature ventricular stimulus produced (1) depression of A-V nodal conduction in the ensuing sinus beat A1 and (2) relative facilitation of A-V nodal conduction of a subsequent premature atrial stimulus (A2). The functional refractory period of the A-V node was reduced when compared with the atrial extrastimulus technique alone.