The functional role of structural complexities in the propagation of depolarization in the atrium of the dog. Cardiac conduction disturbances due to discontinuities of effective axial resistivity.

Spach, Madison S.; Miller, W. Thomas; Dolber, Paul C.; Kootsey, J. Mailen; Sommer, J.; Mosher, C. E.

doi:10.1161/01.res.50.2.175

Cited by 512 publications

(234 citation statements)

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“…Ten Eick and Singer (1979) also reported that diseased atria were hypopolarized with respect to normal atria (Gelband et al 1972) and that the difference in the membrane potentials of closely adjacent cells could be much larger in diseased than in normal atria. Recently Spach et al (1982) reported that structural complexities markedly affected the velocity and the safety factor of propagation in atrial muscle. Discontinuities of effective axial resistivity due to structural complexities result in multiple conduction disturbances in the atrium.…”

Section: Discussionmentioning

confidence: 99%

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Split atrial activity in a man with Brady-Tachy syndrome.

Oda

Shibuya

Satoh

et al. 1983

Tohoku J. Exp. Med.

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A 74-year-old man with brady-tachy syndrome showed split atrial activities in electrophysiologic studies. The split intervals of atrial activities varied spontaneously or in response to electric stimulations.The shorter were the coupling intervals of atrial extrastimuli, the longer the split intervals of captured atrial activities.At a critical timing of atrial extrastimuli, atrial flutter-fibrillation was initiated reproducibly. During atrial flutter-fibrillation, the split activities showed Wenckebach-like phenomenon. These findings seem to result from depressed conductivity.The split atrial activity may reflect a diseased state of the atrium which predisposes to atrial arrhythmias.-split atrial activity; diseased atrium; atrial arrhythmia; brady-tachy syndrome; atrial flutter-fibrillation

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Section: Discussionmentioning

confidence: 99%

“…Under normal conditions, enough depolarizing current is coupled across such discontinuities to maintain propagation. However, when the maximum membrane depolarizing current was reduced by increasing the extracellular potassium concentration or by premature stimulation, block occurred at these sites (Spach et al 1982).…”

Section: Discussionmentioning

confidence: 99%

Split atrial activity in a man with Brady-Tachy syndrome.

Oda

Shibuya

Satoh

et al. 1983

Tohoku J. Exp. Med.

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“…If there were two discrete deflections for one atrial complex in the ECG (ie, a so-called double potential), the activation time at these sites was assigned to the deflection with the highest amplitude for bipolar electrograms or the more rapid deflection for unipolar electrograms. 36,37 Because the size of the right atrium differed from dog to dog, anatomic landmarks (vena cavae, right atrial appendage, AV groove) were identified and positioned on the grid (electrode array) by visual inspection. For each atrial beat, activation time at each site was placed on an anatomic grid representing activation at each bipolar recording site, and isochronous lines at 10 and then terminated the atrial flutter 5 minutes 30 seconds after starting its administration.…”

Section: Moricizine Study Protocolmentioning

confidence: 99%

Mechanism of interruption of atrial flutter by moricizine. Electrophysiological and multiplexing studies in the canine sterile pericarditis model of atrial flutter.

et al. 1994

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BACKGROUND Moricizine is said to have potent effects on cardiac conduction but little or no effect on cardiac refractoriness. METHODS AND RESULTS The effects of moricizine (2 mg/kg IV) on induced atrial flutter were studied 2 to 4 days after the creation of sterile pericarditis in 11 dogs. Ten episodes of stable atrial flutter before and after the administration of moricizine were studied in 9 dogs in the conscious, nonsedated state, and 7 episodes were studied in 6 dogs in the anesthetized, open chest state. In the conscious state, the effects of moricizine on atrial excitability, atrial effective refractory period, and intra-atrial conduction times were studied by recording during overdrive pacing of sinus rhythm from epicardial electrodes placed at selected atrial sites. Moricizine prolonged the atrial flutter cycle length in all the episodes, from a mean of 133 +/- 9 to 172 +/- 27 milliseconds (P < .001), and then terminated 7 of the 10 episodes. Moricizine increased the atrial threshold of excitability from a mean of 2.3 +/- 1.4 to 3.3 +/- 2.2 mA (P < .01) and prolonged intra-atrial conduction times (measured from the sulcus terminalis to the posteroinferior left atrium) from a mean of 58 +/- 6 to 64 +/- 5 milliseconds (P < .005). Prolongation of the atrial effective refractory period from 166 +/- 20 to 174 +/- 24 milliseconds (P < .05) was observed only at the sulcus terminalis site. In the open chest studies, administration of moricizine prolonged the atrial flutter cycle length from a mean of 150 +/- 15 to 216 +/- 30 milliseconds (P < .001) and then terminated the atrial flutter in all 7 episodes. As demonstrated by simultaneous multisite mapping from 95 bipolar sites on the right atrial free wall, the atrial flutter cycle length prolongation was either due to further slowing of conduction in an area of slow conduction in the reentrant circuit of the atrial flutter (5 episodes) or further slowing of conduction in an area of slow conduction plus the development of a second area of slow conduction (2 episodes). The change in conduction times in the rest of the reentrant circuit was negligible (10.9 +/- 8.7% of the total change). In all 7 episodes, the last circulating reentrant wave front blocked in an area of slow conduction. CONCLUSIONS Moricizine (1) prolongs the atrial flutter cycle length, primarily by slowing conduction in an area of slow conduction in the reentrant circuit, (2) terminates atrial flutter by causing block of the circulating reentrant wave front in an area of slow conduction of the reentrant circuit, and (3) effectively interrupts otherwise stable atrial flutter in this canine model. The reason for these effects of moricizine are not readily explained by its effects on global atrial conduction times and refractoriness studied during sinus rhythm. Local changes in conduction in an area(s) of slow conduction are responsible for both cycle length prolongation and atrial flutter termination rather than the traditional wavelength concept of head-tail interaction.

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“…The dismally connected fibers in infected myocardial tissue with continuous fibro-degenerative modification may induce anomalous electrophysiological characteristics. Electrical coupling between adjacent fibers is difficult to occur when fibrosis surrounds groups of myocytes [1][2][3][4]. The microarchitecture and anisotropic characteristics may play an important role in re-entry by causing inhomogeneous and discontinuous propagation of the impulse.…”

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confidence: 99%