Atrioventricular Nodal Conduction Rather than Automaticity Determines the Ventricular Rate During Atrial Fibrillation and Atrial Flutter

ANDRAS VERECKEI, ZAK VERA, HARALD P. PRIDE, DOUGLAS P. ZIPES

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

AV Nodal Conduction During Atrial Fibrillation and Flutter. Introduction: Recent clinical studies have advanced the hypothesis that the atrioventricular (AV) node does not conduct cardiac impulses, but functions as a pacemaker whose discharge rate and rhythm are modulated electrotonically by atrial impulses. Major support for the hypothesis comes from the observation that the short ventricular cycles during atrial fibrillation can be totally eliminated by ventricular pacing at relatively long ventricular cycle lengths. Methods and Results: The hypothesis was tested in ten anesthetized open chest mongrel dogs with sustained atrial fibrillation or atrial flutter (AF). Large differences (> 120 msec) between the ventricular pacing cycle length that achieved > 95% ventricular capture and the shortest spontaneous RR cycle during AF were considered to be consistent with the modulated AV nodal pacemaker hypothesis, while values ≤ 120 msec were not. The results showed that the ventricular pacing cycle length capturing > 95% of ventricular complexes during AF depended on the spontaneous ventricular rate during AF. Short spontaneous RR cycles during AF required short ventricular pacing cycle lengths to achieve > 95% capture, and the difference between the ventricular pacing cycle length and the shortest spontaneous RR cycle length was narrow, i.e., ≤ 120 msec. Slower ventricular rates could be captured at longer ventricular pacing cycle lengths, and the difference between the ventricular pacing cycle length capturing > 95% of the ventricular complexes and the shortest spontaneous RR interval during AF was large, i.e., > 120 msec. A continuum existed, and values ≤ 120 msec could be transformed to values > 120 msec by increasing vagal intensity to slow the ventricular response. We also found in five dogs that we could not achieve overdrive suppression of automaticity of the putative AV nodal pacemaker focus by ventricular pacing at various cycle lengths and durations during atrial fibrillation. Conclusion: In conclusion, data from this study fail to support the modulated AV nodal pacemaker hypothesis and are more consistent with conventional concepts of AV nodal conduction.

Original languageEnglish (US)
Pages (from-to)534-543
Number of pages10
JournalJournal of Cardiovascular Electrophysiology
Volume3
Issue number6
DOIs
StatePublished - Dec 1992

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Atrial Flutter
Atrial Fibrillation
Dogs
Atrioventricular Node
Thorax

Keywords

  • atrioventricular nodal function
  • concealed conduction
  • modulated atrioventricular nodal pacemaker
  • ventricular rate of atrial rhythms

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Atrioventricular Nodal Conduction Rather than Automaticity Determines the Ventricular Rate During Atrial Fibrillation and Atrial Flutter. / VERECKEI, ANDRAS; VERA, ZAK; PRIDE, HARALD P.; ZIPES, DOUGLAS P.

In: Journal of Cardiovascular Electrophysiology, Vol. 3, No. 6, 12.1992, p. 534-543.

Research output: Contribution to journalArticle

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abstract = "AV Nodal Conduction During Atrial Fibrillation and Flutter. Introduction: Recent clinical studies have advanced the hypothesis that the atrioventricular (AV) node does not conduct cardiac impulses, but functions as a pacemaker whose discharge rate and rhythm are modulated electrotonically by atrial impulses. Major support for the hypothesis comes from the observation that the short ventricular cycles during atrial fibrillation can be totally eliminated by ventricular pacing at relatively long ventricular cycle lengths. Methods and Results: The hypothesis was tested in ten anesthetized open chest mongrel dogs with sustained atrial fibrillation or atrial flutter (AF). Large differences (> 120 msec) between the ventricular pacing cycle length that achieved > 95{\%} ventricular capture and the shortest spontaneous RR cycle during AF were considered to be consistent with the modulated AV nodal pacemaker hypothesis, while values ≤ 120 msec were not. The results showed that the ventricular pacing cycle length capturing > 95{\%} of ventricular complexes during AF depended on the spontaneous ventricular rate during AF. Short spontaneous RR cycles during AF required short ventricular pacing cycle lengths to achieve > 95{\%} capture, and the difference between the ventricular pacing cycle length and the shortest spontaneous RR cycle length was narrow, i.e., ≤ 120 msec. Slower ventricular rates could be captured at longer ventricular pacing cycle lengths, and the difference between the ventricular pacing cycle length capturing > 95{\%} of the ventricular complexes and the shortest spontaneous RR interval during AF was large, i.e., > 120 msec. A continuum existed, and values ≤ 120 msec could be transformed to values > 120 msec by increasing vagal intensity to slow the ventricular response. We also found in five dogs that we could not achieve overdrive suppression of automaticity of the putative AV nodal pacemaker focus by ventricular pacing at various cycle lengths and durations during atrial fibrillation. Conclusion: In conclusion, data from this study fail to support the modulated AV nodal pacemaker hypothesis and are more consistent with conventional concepts of AV nodal conduction.",
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