Cellular electrophysiologic characteristics of chronically infarcted myocardium in dogs susceptible to sustained ventricular tachyarrhythmias

Spear, Joseph F.; Michelson, Eric L.; Moore, E. Neil

doi:10.1016/s0735-1097(83)80112-0

Cited by 124 publications

(50 citation statements)

References 31 publications

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“…We have previously subjected tissues obtained in a similar manner to histological examination to confirm our ability to obtain parallel fiber orientation over the length of the tissue. 18 In addition, the typical elliptical isochronal pattern identified in vitro correlates excellently with the direction of myocardial fibers.…”

Section: Tissue Preparationmentioning

confidence: 78%

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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Section: Tissue Preparationmentioning

confidence: 78%

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

et al. 1988

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“…Our techniques have been described in detail previously. 20 Transmembrane action potentials were recorded from cells in the superficial layers of the epicardial preparations with standard 3M potassium-filled microelectrodes. The potential was stable for 45 to 60 sec before data acquisition.…”

Section: Methodsmentioning

confidence: 99%

The cellular electrophysiologic changes induced by high-energy electrical ablation in canine myocardium.

Levine¹,

Spear²,

Weisman³

et al. 1986

Circulation

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High-energy electrical ablation is a new experimental approach to control arrhythmias. In this study, the cellular electrophysiologic effects of high-energy shocks (5 to 40 J) delivered in vitro to 14 epicardial tissues from 11 dogs were studied in an attempt to understand the nature and extent of injury as well as potential arrhythmogenic mechanisms. In addition, this preparation was used to test the importance of cathode-anode configuration, current density, and fiber orientation in the induction of tissue injury in vitro. Electrophysiologic abnormalities were noted up to 10 mm from the electrode wall, and their extent was determined in part by current density and the cathode-anode orientation. A decrease in resting membrane potential, action potential amplitude, and dV/dT occurred in all tissues after high-energy shocks, which was worst nearest the cathode and of graded severity at increasing distances from the cathode. The most severe effects were noted with high current densities and in tissues located between the cathode and anode. In addition, impaired impulse conduction and abnormal repolarization were documented. Histologic study demonstrated contraction band necrosis immediately after delivery of high-energy shocks. The extent and distribution of the contraction bands was in part dependent on the energy delivered and the cathode-anode configuration. These findings suggest potential mechanisms for arrhythmogenesis and altered regional hemodynamic abnormalities that occur in vivo.

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“…An epicardial strip 2 mm thick from beneath the plaque was then removed, mounted in the tissue bath, and superfused with oxygenated Tyrode's solution at 370 C. A period of 60 min was allowed for equilibration before proceeding with the electrophysiologic examination in vitro for the reasons described previously. 19 Bipolar stimulating electrodes were placed at each end of the epicardial strip, and a fixed bipolar reference recording electrode was placed at a convenient location on the strip. A roving bipolar electrode (0.6 mm interelectrode distance) was used to record local electrograms over the surface of the strip.…”

Section: Methodsmentioning

confidence: 99%

Electrophysiologic substrate for ventricular tachycardia: correlation of properties in vivo and in vitro.

Richards¹,

Blake²,

Spear³

et al. 1984

Circulation

122

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Cardiac electrophysiologic studies were performed in three control dogs and in nine dogs with previous (8 to 22 days) anterior myocardial infarction. During programmed stimulation, no control dog had inducible ventricular fibrillation (VF) or tachycardia (VT); three dogs with infarcts had inducible VF and six had inducible VT. Recordings in vivo were made via a plaque electrode containing 10 bipolar electrodes (3.0 x 1.5 cm) placed on the epicardial surface of the anteroapical left ventricle. Subsequently, epicardial strips (2 mm thick) from beneath the plaque were prepared for studies in vitro. Electrogram durations were significantly greater in dogs with infarcts than in control dogs both in vivo (p < .05) and in vitro (p < .00 1). Electrogram amplitudes were significantly lower in dogs with VT in vivo (p < .05) and in vitro (p < .001). In control animals activation was continuous and most rapid in the direction of fiber orientation; there were areas of slow and/or discontinuous conduction in all dogs with infarcts. In one case, sustained reentrant beating in vitro was caused by functional unidirectional block and microreentry at a site of continuous electrical activity during VT in vivo. Reentrant beating in vitro persisted in 0.5 cc of isolated tissue. We conclude that broad lowamplitude electrograms in vivo and in vitro depict local areas of slow and/or discontinuous conduction, that the intrinsic asymmetry of cardiac activation due to fiber orientation is accentuated by infarction and may predispose to intraventricular reentry, and that intraventricular reentrant circuits that may be present on the epicardial surface may persist in a volume of myocardial tissue as small as 0.5 cc. Circulation 69, No. 2, 369-381, 1984. ALTHOUGH the electrophysiologic basis for ventricular tachycardia (VT) in the context of chronic myocardial infarction usually is thought to be reentry, 1-9 the size and nature of intraventricular reentrant circuits remain to be determined. It has been shown that broad fractionated electrograms that can often be recorded in vivo at the edge of infarcts8 may be associated with reentrant circuits. Electrophysiologic abnormalities observed in vitro and pathologic changes have been implicated as constituents of the substrate for VT.1020 However, none of these reports has described the spatial relationships of the properties in vivo and in vitro. Consequently, there remains a gap in our knowledge of the exact nature of the electrophysiologic substrate for VT. We have used a canine preparation of experimental myocardial infarction to try to bridge this gap.The purposes of the present study were to establish the relationship between electrophysiologic properties in vivo and in vitro in dogs with and without inducible VT and to determine the nature of the electrophysiologic substrate for this condition.

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Cellular electrophysiologic characteristics of chronically infarcted myocardium in dogs susceptible to sustained ventricular tachyarrhythmias

Cited by 124 publications

References 31 publications

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

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

The cellular electrophysiologic changes induced by high-energy electrical ablation in canine myocardium.

Electrophysiologic substrate for ventricular tachycardia: correlation of properties in vivo and in vitro.

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