Mechanism of Synchronization in Isorhythmic Dissociation

Levy, Matthew N.; Zieske, Harrison

doi:10.1161/01.res.27.3.429

Cited by 34 publications

(17 citation statements)

References 32 publications

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“…We agree with Levy and Z ieske [10] that variations of blood pressure play an important part in the biological control system which leads to a synchronization of ventricular and atrial rhythm, either by baroreccptor reflex or by influencing the pressure in the sinus node artery directly [7,8]. In view of the results of Paulay et al [13] and Paulay and Damato [14], we must concede a certain influence of right atrial pressure level upon sinus rate in isorhythmic dissociation and similar conditions.…”

Section: Discussionsupporting

confidence: 85%

“…[7], a direct influence of the pressure in the sinus node artery on sinus rate must be taken into consideration. In our experiments, in con trast to the study of Levy and Z ieske [10], synchronization did not cease when the aortic pressure was kept at a constant level ( fig. 3, 4), indicating that synchronization of different rhythms can occur independently from fluctuations in arterial pressure.…”

Section: Discussionsupporting

confidence: 61%

“…Recently, Levy and Z ieske [10], Paulay et til. [13] and Paulay and Damato [14] have reported experimental studies in dogs and humans.…”

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confidence: 98%

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Mechanism of Synchronization in Isorhythmic Dissociation

Diederich¹,

Djonlagić²

1973

Cardiology

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Synchronization of atria and ventricles resembling the clinical phenomenon of isorhythmic A-V dissociation could be produced in 45 of 48 anesthetized cats by stimulating the ventricles slightly above the spontaneous sinus rate. A fall in aortic pressure connected with an increase in right atrial pressure always occurred when ventricular contraction preceded atrial contraction. Synchronization could be prevented neither by vagotomy or β-adenolysis nor by keeping the right atrial or aortic pressure at a constant level. Stretching of the sinus node fibers during atrial contraction against a closed tricuspid valve is regarded as the crucial mechanism responsible for A-V synchronization.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionsupporting

confidence: 61%

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Mechanism of Synchronization in Isorhythmic Dissociation

Diederich¹,

Djonlagić²

1973

Cardiology

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“…Finally, as suggested by Levy et al (Levy and Zieske, 1970;Levy and Edflstein, 1970) one additional role for vagally mediated entrainment and phaselocking of pacemaker periodicity can be found in the distinct harmonic relations between sinoatrial and ventricular frequencies in some patients with complete AV dissociation (isorhythmic dissociation).…”

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confidence: 86%

Dynamic vagal control of pacemaker activity in the mammalian sinoatrial node.

Jalife¹,

Slenter²,

Salata³

et al. 1983

Circulation Research

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SUMMARY. Dynamic heart rate control by parasympathetic nervous input involves feedback mechanisms and reflex bursting of efferent cardiac vagal fibers. Periodic vagal bursting induces phasic changes in sinoatrial cycle length and can entrain the pacemaker to beat at periods that may be identical to those of the vagal burst. We investigated the electrophysiological basis of these phenomena in isolated sinus node preparations (rabbit, cat, and sheep). In the presence of propranolol (3.9 X 10~6 M), relatively brief (50-150 msec) trains of stimuli, applied onto the endocardial surface of the preparation, activated postganglionic vagal terminals and induced a brief hyperpolarization of sinoatrial pacemaker cells. This vagally mediated hyperpolarization could alter the pacemaker rhythm by an amount that depended on its duration and its position in the cycle, as well as on the duration of the free-running pacemaker period. When the free-running period was sufficiently long and the hyperpolarization was induced sufficiently early in the spontaneous cycle, a "paradoxical" acceleration of the pacemaker rhythm ensued. Phasic changes were plotted on phase-response curves, constructed by scanning systematically the sinoatrial pacemaker period with single or repetitive vagal trains. These phase-response curves enabled us to predict the entrainment characteristics and the levels of synchronization of the pacemaker to the vagal periodicity. The overall data explain the cellular mechanisms involved in the phasic effects of brief vagal discharges on sinoatrial periodicity, and provide conclusive evidence for the prediction that repetitive vagal input is capable of forcing the cardiac pacemaker to beat at rates that can be faster or slower than the intrinsic pacemaker rate. These data should improve our knowledge of the dynamic control of heart rate by neural reflexes and aid in our understanding of rhythm disturbances generated by the interaction of the cardiac pacemaker with vagal activity. (Circ Res 52: 642-656, 1983)

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“…However, under physiological circumstances, brief vagal pulses are phase-locked to the cardiac cycle as a result of the pressure wave activating the carotid baroreceptors. 30 This "phaselocked" vagal perturbation might also give rise to irregular dynamics. Indeed, in a previous publication, 3 we reported results of simulations wherein vagal pulses were applied to a single sinoatrial pacemaker at a fixed time after the upstroke of the sinoatrial action potential.…”

Section: Physiological Significancementioning

confidence: 99%

Chaotic activity in a mathematical model of the vagally driven sinoatrial node.

Michaels

Chialvo

Matyas

et al. 1989

Circulation Research

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Phase-locking behavior and irregular dynamics were studied in a mathematical model of the sinus node driven with repetitive vagal input. The central region of the sinus node was simulated as a 15 x 15 array of resistively coupled pacemakers with each cell randomly assigned one of 10 intrinsic cycle lengths (range 290-390 msec). Coupling of the pacemakers resulted in their mutual entrainment to a common frequency and the emergence of a dominant pacemaker region. Repetitive acetylcholine (ACh; vagal) pulses were applied to a randomly selected 60% of the cells. Over a wide range of stimulus intensities and basic cycle lengths, such perturbations resulted in a large variety of stimulus/response patterns, including phase locking (1 ; 1,3 : 2, 2 : 1 , etc.) and irregular (i.e., chaotic) dynamics. At a low ACh concentration (1 fiM), the patterns followed the typical Farey sequence of phase-locked behavior. At a higher concentration (5 ftM), period doubling and aperiodic patterns were found. When a single pacemaker cell was perturbed with repetitive ACh pulses, qualitatively similar results were obtained. In both types of simulation, chaotic behavior was investigated using phase-plane ( Received December 7, 1988; accepted June 2,1989. randomly selected 20% of the cells. Such external perturbation resulted in a shift of the dominant pacemaker site and a decrease in apparent conduction velocity within the pacemaker array, which mimicked very accurately the response patterns of the mammalian heart rate to vagus nerve stimulation. 6 -7 Repetitive vagal input is capable of entraining the already mutually entrained pacemaker array in a harmonic fashion similar to that seen previously 4 for single cells. In fact, depending on the frequency of the ACh input, zones of stable phase-locking rhythms (1 : 1,2:1, etc.) may be separated by regions in which extremely irregular behavior can predominate. Several questions arise from the study of these phenomena that may have importance in the quantitative description of the heart rhythm and its alterations. First, is it possible to analyze and describe this very complex aperiodic behavior in a quantitative but nonstatistical form? Second, can the transition ("road") between ordered (i.e., 1 : 1,

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Mechanism of Synchronization in Isorhythmic Dissociation

Cited by 34 publications

References 32 publications

Mechanism of Synchronization in Isorhythmic Dissociation

Mechanism of Synchronization in Isorhythmic Dissociation

Dynamic vagal control of pacemaker activity in the mammalian sinoatrial node.

Chaotic activity in a mathematical model of the vagally driven sinoatrial node.

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