An experimental study of concealed conduction

Moe, Gordon K.; Abildskov, J.A.; Méndez, Carlos

doi:10.1016/0002-8703(64)90008-0

Cited by 155 publications

(106 citation statements)

References 13 publications

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“…This study, as well as our previous study, demonstrates that the electrophysiological explanation for concealed conduction, as offered by Langendorf and later experimentally confirmed does not seem to be applicabie in patients with AF and seemingly normal AV behavior (Langendorf, 1948;Moe, et al, 1964;Langendorf, et al, 1965;Moore, 1967 ;Moore, et al, 1971;Mazgalev, et al, 1982;Dreifus and Mazgalev, 1988). While random ventricular rhythm in AF should be contributed to the random input by the fibrillating atria, the scaling down of the atrial rate does not seem to be caused by decremental conduction and extinction of atrial impulses at different levels within the AV node.…”

Section: Concealed Conduction In Atrial Fibrillationsupporting

confidence: 70%

“…This observation challenges the classical concept that graded properties of the AV node cause decremental conduction and extinction of atrial impulses at different levels within the node (Langendorf, 1948; Moe, et al, 1964;Langendorf, et al, 1965;Moore, 1967;Moore, et al, 1971;Mazgalev, et al, 1982;Dreifus and Mazgalev, 1988) and provides supportive evidence for the hypothesis that during AF the AV node behaves as the pacemaker for the ventricles (Wittkampf, et al, 1988;Meijler and Fisch, 1989).…”

Section: Discussionmentioning

confidence: 75%

“…The classical explanation of the compensatory pause is that concealed retrograde invasion lengthens AV nodal refractory period (Langendorf, 1948;Moe, et al, 1964;Langendorf, et al, 1965;Moore, 1967;Dreifus and Mazgalev, 1988) . This lengthening then would have to be equal to the sum of the RS interval and the relative shift of the histogram of SR intervals.…”

Section: Lengthening Of a V Nodal Refraetorinessmentioning

confidence: 99%

“…The rate and irregularity of the ventricular rhythm in atrial fibrillation (AF) is generally thought to result from decremental conduction and extinction of anterograde fibrillatory impulses at different levels within the atrioventricular (AV) node (Langendorf, 1948;Moe, et al, 1964;Langendorf, et al, 1965;Moore, 1967; Manuscript received 13 April 1990; Accepted for publication 2 July 1990. Mazgalev, et al, 1982;Dreifus and Mazgalev, 1988) .…”

Section: Introductionmentioning

confidence: 99%

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Atrioventricular Nodal Response to Retrograde Activation in Atrial Fibrillation

Wittkampf

Jongste²,

Meijler

1990

Cardiovasc electrophysiol

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. Atrioventricular Nodal Reset. Retrograde (ventriculoatrial) conduction that reaches the atrioventricular node simultaneous with, or just before an atrial impulse can facilitate subsequent anterograde conduction. However, a spontaneous or programmed ventricular extrasystole during atrial fibrillation is generally followed by a compensatory pause indicating subsequent delayed anterograde transmission. This characteristic response was used as a model to study the mechanism of atrioventricular no dal behavior during atrial fibrillation. In eight medically-treated patients with chronic atrial fibrillation and a relatively slow but random ventricular response, single premature right ventricular stimuli were delivered after every eighth spontaneous R wave during at least 1 hour~ A fixed coupling interval of the extrastimulus, considerably shorter than the shortest spontaneous RR interval, was used. The histograms of the postextrasystolic intervals were compared with those of the spontaneous noninterrupted RR intervals. The average postextrasystolic interval was 180 to 300 msec longer than the mean control RR interval, and in six of eight patients, the shape of the histogram of the postextrasystolic cycles was insignificantly different from that of the spontaneous RR intervals. This suggests that in those six patients, the retrogradeimpulse had reset the random timing cycle of atrioventricular nodal dis charge during atrial fibrillation. This observation is compatible with the hypothesis that electrotonically-mediated propagation across a weakly coupled junctional area within the atrioventricular node, rather than decremental conduction and extinction of anterograde atrial impulses at different levels within the node, may be the mechanism of atrioventricular transmission in atrial fibrillation.

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Section: Concealed Conduction In Atrial Fibrillationsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 75%

Section: Lengthening Of a V Nodal Refraetorinessmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Atrioventricular Nodal Response to Retrograde Activation in Atrial Fibrillation

Wittkampf

Jongste²,

Meijler

1990

Cardiovasc electrophysiol

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“…However, the precise mechanism of concealed (anterograde and retrograde) conduction is still not clear. On one hand, these phenomena have been explained by gradually changing properties of the AV node (Langendorf, 1948;Moe, et al, 1964;Langendorf, et al, 1965;Moore, 1967;Lehmann, et al, 1984). Others have hypothesized This study was supported by the Wijnand M .…”

Section: Introductionmentioning

confidence: 73%

Competitive Anterograde and Retrograde Atrioventricular Junctional Activation in Atrial Fibrillation

Wittkampf

Jongste²,

Meijler

1990

Cardiovasc electrophysiol

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Reset and Cancellation. In eight medically-treated patients with chronic atrial fibrillation and a random ventrÏcular rhythm, we studied the effect of single right ventricular stimuli delivered af ter each eighth spontaneous R wave during at least 1 hour. The coupling interval of the extrastimulus was fixed and differed marginally from the shortest spontaneous RR interval. The histograms of spontaneous RR intervals and of the "compensatory" pauses following the ventricular extrasystoles were calculated. Analysis of these histograms and simulation of the interaction between anterograde and retrograde impulses in a computer model suggests that in seven of the eight patients the compensatory pause may be caused by two distinctly different mechanisms: (1) reset of the timing cycle of atrioventricular no dal activation by relatively early retrograde impulses; and (2) interception of anterograde impulses by relatively late ventricular extrasystoles. The finding that early retrograde impulses are not blocked by concealed atrioventricular no dal conduction makes the existence of decremental conduction and extinction of atrial impulses at different levels within the node unlikely. The results ofthis study support the hypothesis that the distal side of a weakly coupled junctional area inside the AV node behaves as a pacemaker for the ventricular rhythm during atrial fibrillation.

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Atrial Fibrillation: Mechanisms, Therapeutics, and Future Directions

Pellman

Sheikh

2015

Comprehensive Physiology

118

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Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, affecting 1% to 2% of the general population. It is characterized by rapid and disorganized atrial activation leading to impaired atrial function, which can be diagnosed on an EKG by lack of a P-wave and irregular QRS complexes. AF is associated with increased morbidity and mortality and is a risk factor for embolic stroke and worsening heart failure. Current research on AF support and explore the hypothesis that initiation and maintenance of AF require pathophysiological remodeling of the atria, either specifically as in lone AF or secondary to other heart disease as in heart failure-associated AF. Remodeling in AF can be grouped into three categories that include: (i) electrical remodeling, which includes modulation of L-type Ca2+ current, various K+ currents and gap junction function; (ii) structural remodeling, which includes changes in tissues properties, size, and ultrastructure; and (iii) autonomic remodeling, including altered sympathovagal activity and hyperinnervation. Electrical, structural, and autonomic remodeling all contribute to creating an AF-prone substrate which is able to produce AF-associated electrical phenomena including a rapidly firing focus, complex multiple reentrant circuit or rotors. Although various remodeling events occur in AF, current AF therapies focus on ventricular rate and rhythm control strategies using pharmacotherapy and surgical interventions. Recent progress in the field has started to focus on the underlying substrate that drives and maintains AF (termed upstream therapies); however, much work is needed in this area. Here, we review current knowledge of AF mechanisms, therapies, and new areas of investigation.

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An experimental study of concealed conduction

Cited by 155 publications

References 13 publications

Atrioventricular Nodal Response to Retrograde Activation in Atrial Fibrillation

Atrioventricular Nodal Response to Retrograde Activation in Atrial Fibrillation

Competitive Anterograde and Retrograde Atrioventricular Junctional Activation in Atrial Fibrillation

Atrial Fibrillation: Mechanisms, Therapeutics, and Future Directions

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