Assessment of refractoriness of the human Purkinje system

Fleischmann, D.; Pop, T.

doi:10.1093/cvr/12.11.681

Cited by 7 publications

(5 citation statements)

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“…In the preceding paragraphs we substantiated our assumption that the prematurely elicited and retrogradely propagating RV impulse Sz will mainly be delayed traversing the distal Purkinje fibers (20,21). Extreme and critical prolongation of the retrograde intraventricular conduction time $2H2, therefore, probably signals critically and extremely reduced conduction velocity of the impulse $2 within the distal Purkinje system.…”

Section: The Origin Of the Repetitive Beats; Re-entry Mechanism Versusupporting

confidence: 71%

“…The striking difference in the duration of the $2H2 intervals after premature RV stimulation during the RV and the RA drive rhythm supports the hypothesis that the main delay of the retrograde conduction time $2H2 is confined in the distal Purkinje system (20,21). If the main delay of retrograde conduction from the site of stimulation within the ventricle to Basic Research in Cardioiogy, VoI.…”

Section: The Conduction Delay During Retrograde Propagation Of Sz Witsupporting

confidence: 58%

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Rate and rhythm dependent vulnerability of the human ventricular myocardium

Fleischmann¹,

Marschall²,

Bakker³

1979

Basic Res Cardiol

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Section: The Origin Of the Repetitive Beats; Re-entry Mechanism Versusupporting

confidence: 71%

Section: The Conduction Delay During Retrograde Propagation Of Sz Witsupporting

confidence: 58%

Rate and rhythm dependent vulnerability of the human ventricular myocardium

Fleischmann¹,

Marschall²,

Bakker³

1979

Basic Res Cardiol

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“…In the steady-state a t frequencies greater than about 60 min-1 there is a pronounced shortening of the action potential (figure 1); evidence of this shortening has been observed in all cardiac tissues studied (Carmeliet 1977;B oyett & Jewell 1980) including human Purkinje fibres (Fleischmann & Pop 1978). This shortening has been shown to occur in the first beat after an increase in the stimulus frequency, and to be removed in the first beat after a rate decrease (figure 2).…”

Section: Action Potential Durationmentioning

confidence: 85%

Activity-dependent changes in the electrical behaviour of sheep cardiac Purkinje fibres

Fedida

Boyett

1985

Proc. R. Soc. Lond. B.

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Rate-dependent changes in the electrical activity of sheep Purkinje fibres maintained at 37 °C have been investigated. The duration of the action potential is maximal at a frequency of about 60 min -1 . When the rate is increased above 60 min -1 there is a substantial shortening of the action potential; this occurs abruptly in the first beat at the higher rate although subsequently there can be further changes in duration and these can result in a small prolongation, no change, or a small further shortening of the action potential and can take up to 10 min to reach a steady-state. When the rate is reduced from 60 min -1 there is also a shortening of the action potential but it occurs gradually over several hundred seconds. Action potential duration reaches a minimum value at a rate of about 6 min -1 . 70% of preparations studied showed an increase in duration again at rates below 6 min -1 but duration is always constant at frequencies below about 0.1 min -1 . The maximum diastolic potential is more negative and the pacemaker potential is larger at higher rates of stimulation. When the frequency is raised these variables increase over a time course lasting several hundred seconds. At rates below 60 min -1 the slow changes in action potential duration, maximum diastolic potential and pacemaker potential, after a change in the stimulus frequency, all have similar monoexponential time courses (Ƭ ≈ 3 min) and are accompanied by slow changes in tension production over a similar time course. In Purkinje fibres that exhibit spontaneous activity, rapid stimulation results in overdrive excitation: an acceleration of spontaneous activity when stimulation is ceased.

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“…In the light of these in vitro experiments we (3,7,8) localize the increasing delay of the retrograde intraventricular conduction time $2H2 ( fig. 2, 3) during premature RV stimulation at the junction of the ventricular myocardium and the distal Purklnje system.…”

Section: The Echo Zonementioning

confidence: 97%

“…During a slow heart rate a long S2H 2 delay was necessary for the induction of the V 3 beat ( fig. 8) (17)(18)(19)(20)7). at BCL of 500 ms the S2H 2 intervals with vulnerability revealed shorter values.…”

mentioning

confidence: 96%

Observations on the mechanism of human ventricular vulnerability during premature stimulation

Fleischmann¹,

T²,

Wiesener³

et al. 1979

Basic Res Cardiol

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Sum_marySpontaneous ventricular extrasystoles (V3-beats) occur frequently after premature ventricular stimuli induced during a paced ventricular rhythm. The V3 phenomenon was observed in, 100 of 158 patients (63.3%) with and without heart disease being studied for the evaluation of various rhythm disorders. In patients with an old myocardial infarction there was an increased tendency to exhibit short ventricular salvos (V3-V 5 beats) after prematurely elicited test pulses. V~-beats occurred less frequently in patients with a bundle branch block than in patients with normal intraventricular conduction.The statistical analysis of several variables obtained during the investigation revealed that the frequency and the appearance time of the V 3 beats and the vulnerable period of the cardiac cycle are related to a critical delay of the retrograde Purkinje-His conduction time of the premature test pulse, the basic rate of the drive rhythm and the state of excitability of the ventricular myocardium. The results strongly suggest a re-entry mechanism generating the spontaneous ventricular extrasystoles. The main delay of conduction of the premature test pulse seems to be localized not within the working myocardial fibers or the proximal His-Purkinje system but rather within the distal Purkinje fiber system. Therefore, the re-entry pathway of the V~ beats is thought to be confined to the right ventricular Purkinje fiber network near the site of stimulation.Clinically, it can be deduced that an artificially induced ventricular re-entry beat is tolerated and extinguished in the stable heart by physiological protective mechanisms. In the diseased heart, however, an increased state of fiber inhomogenity may be generated by the V 3 beat leading to recurrent re-entry impulses.Premature right ventricular stimulation during a paced ventricular rhythm has become a routine procedure in clinical electrophysiology. Early test pulses may lead to spontaneous ventricular extrasystoles. These beats have to be considered as a variant form of human ventricular vulnerability. Usually, only one spontaneous ventricular extrasystole *) Supported by Deutsche Forschungsgemeinschaft SFB 109 807

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Assessment of refractoriness of the human Purkinje system

Cited by 7 publications

References 0 publications

Rate and rhythm dependent vulnerability of the human ventricular myocardium

Rate and rhythm dependent vulnerability of the human ventricular myocardium

Activity-dependent changes in the electrical behaviour of sheep cardiac Purkinje fibres

Observations on the mechanism of human ventricular vulnerability during premature stimulation

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