The discontinuous nature of propagation in normal canine cardiac muscle. Evidence for recurrent discontinuities of intracellular resistance that affect the membrane currents.

Spach, Madison S.; Miller, W. Thomas; Geselowitz, David B.; Barr, Roger C.; Kootsey, J. Mailen; Johnson, Edward A.

doi:10.1161/01.res.48.1.39

Cited by 706 publications

(314 citation statements)

References 39 publications

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“…This anisotropy can be explained by the anisotropic conductivity of cardiac muscle (Clerc, 1976;Roberts et al, 1979). It has been suggested recently (Spach et al, 1981) that anisotropy of conduction may be important in arrhythmias.…”

Section: Department Of Physiology and Biophysics University Of Washimentioning

confidence: 99%

Effect of tissue anisotropy on extracellular potential fields in canine myocardium in situ.

Roberts¹,

Scher²

1982

Circulation Research

239

159

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SUMMARY. The extracellular epicardial potential fields produced by simple depolarization waves in the in situ canine left ventricular myocardium were analyzed. A mathematical model that included tissue anisotropy was developed to explain the observed fields. Values of intracellular (i), extracellular (o), longitudinal (f), and transverse (t) resistivity which gave the best fit between the model and experimental data were (in ohm-cm, mean ± SD): r,,, = 852 ± 232, r,,, = 1247 ± 210, r,, = 291 ± 38, rii = 1677 ± 331. The potential fields around simple stimulated waves on the epicardium can best be explained if the extracellular wavefront voltage is (mean ± SD) 74 ± 7 mV for a wave propagating parallel to the local muscle fibers, and 43 ± 6 mV for a wave propagating perpendicular to these fibers. We conclude that the anisotropy of the electrical conductivity of cardiac muscle has important effects on the propagation of waves of depolarization and on the potential fields produced by depolarization in the intact heart. (Circ Res 50: 342-351, 1982)

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Section: Department Of Physiology and Biophysics University Of Washimentioning

confidence: 99%

Effect of tissue anisotropy on extracellular potential fields in canine myocardium in situ.

Roberts¹,

Scher²

1982

Circulation Research

239

159

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“…(Circulation 1988;78:1478-1494 S low conduction and unidirectional block are requirements for reentrant pathways.1-9 In addition to slow conduction because of a decrease in the rate of rise of the intracellular potential, differences in cell-to-cell coupling and the geometric arrangement of fibers in cardiac tissue may also produce slow conduction. [10][11][12][13][14][15] pathway defined by fixed areas of block could provide a long enough conduction pathway to allow sufficient time for an impulse conducting at a normal velocity to return to fully recovered cardiac tissue. The extent of increased conduction time distal to anatomic barriers in cardiac tissue has not been extensively investigated.…”

mentioning

confidence: 99%

Interaction of fiber orientation and direction of impulse propagation with anatomic barriers in anisotropic canine myocardium.

et al. 1988

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We developed a computer model of the interaction of impulse propagation with anatomic barriers in uniformly anisotropic tissue. Its predictions were confirmed experimentally by using an in vitro cut to create a 6x 1-mm anatomic barrier in 12 canine epicardial strips. The model predicted that long, thin barriers located parallel to the direction of impulse propagation would have little effect in delaying conduction regardless of the arrangement of cardiac fibers. In this situation, the mean experimental ratio of postcut to control conduction times across the barrier was 1.05:1.00 in 10 tissues. When impulses were proceeding perpendicular to an anatomic barrier, significant distal conduction delay was predicted and found to occur only when the conduction from pacing to recording sites was initially longitudinal to fiber orientation (mean experimental ratio, 2.34: 1.00 in five tissues) but not transverse to fiber orientation (ratio, 1.08: 1.00 in five tissues). We conclude that the direction of initial impulse propagation and the orientation of myocardial fibers have large effects on the degree to which anatomic barriers delay activation in cardiac tissue. These findings may have implications for the participation of anatomic barriers in reentrant circuits. (Circulation 1988;78:1478-1494 S low conduction and unidirectional block are requirements for reentrant pathways.1-9 In addition to slow conduction because of a decrease in the rate of rise of the intracellular potential, differences in cell-to-cell coupling and the geometric arrangement of fibers in cardiac tissue may also produce slow conduction. [10][11][12][13][14][15] pathway defined by fixed areas of block could provide a long enough conduction pathway to allow sufficient time for an impulse conducting at a normal velocity to return to fully recovered cardiac tissue. The extent of increased conduction time distal to anatomic barriers in cardiac tissue has not been extensively investigated. In addition, the consequences of the interrelation of fixed anatomic barriers and tissue anisotropy are unknown. Such activation delay distal to a barrier may have important implications for the participation of a barrier in reentrant circuits.Therefore, we developed a computer model of the interaction of fixed anatomic barriers with conduction in anisotropic tissue. Our goals were to verify the hypotheses that the direction of impulse propagation and the orientation of fibers relative to a fixed anatomic area of block were crucial in determining the degree of conduction delay and perturbation of activation patterns produced distal to the block. We then validated the predictions of this computer analysis in a simple model of anatomic barrier in canine epicardium produced by a thin surgical cut in an in vitro preparation. Materials and Methods Model of Conduction and Anisotropic TissueDirectional differences in conduction velocity in canine myocardium related to fiber orientation have

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“…18,19) In this study, pacing from the CS before RFA resulted in RS or rS unipolar electrograms in the CTI. After RFA with complete CTI block (group 1), the paced wavefront propagated around the TA to the other side of the ablation line.…”

Section: Criteria Of Complete Cti Conduction Blockmentioning

confidence: 62%

Characteristics of Virtual Unipolar Electrogram Voltage and Characteristics of Isthmus Block during Radiofrequency Ablation of Typical Atrial Flutter

Takahashi

Watanabe

Kofune

et al. 2015

Nichidai Igaku Zasshi

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Background:The optimal technique for recording of the electrogram to detect complete cavo-tricuspid isthmus (CTI) block during radiofrequency ablation (RFA) of the typical atrial flutter (AFL) using non-contact mapping system remains unclear. The aim of this study was to investigate the characteristics of the local virtual unipolar electrogram recorded at the ablation line during coronary sinus pacing after RFA of the CTI.Methods: Non-contact mapping was performed in 8 patients with AFL. Non-contact virtual unipolar electrograms were obtained before and after CTI linear ablation. All unipolar electrograms were acquired with both wide-band (0.5-300 Hz and 0.5-IC 150 Hz) and narrow-band filtering (32-300 Hz). The unipolar electrogram measurements included both the peak-to-peak voltage and peak-negative voltage for both filter settings, and the morpho logical characteristics of the second component of double potentials.Results: Comparison of the electrogram voltage along the ablation line before and after ablation demonstrated: 1) peak-negative voltage reduction at the mid-portion of the ablation line by 0.5-IC 150 Hz filtering, and 2) the second component of unipolar electrogram morphologies of R, Rs or rSR were the most sensitive and specific recording technique to predict conduction block.Conclusions: Non-contact unipolar electrograms using the peak-negative voltage with 0.5-IC 150 Hz and a predominant R-wave pattern in the second component at the ablation line indicate complete CTI block, even in the presence of transcristal conduction.

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The discontinuous nature of propagation in normal canine cardiac muscle. Evidence for recurrent discontinuities of intracellular resistance that affect the membrane currents.

Cited by 706 publications

References 39 publications

Effect of tissue anisotropy on extracellular potential fields in canine myocardium in situ.

Effect of tissue anisotropy on extracellular potential fields in canine myocardium in situ.

Interaction of fiber orientation and direction of impulse propagation with anatomic barriers in anisotropic canine myocardium.

Characteristics of Virtual Unipolar Electrogram Voltage and Characteristics of Isthmus Block during Radiofrequency Ablation of Typical Atrial Flutter

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