Virtual Electrode Effects in Transvenous Defibrillation‐Modulation by Structure and Interface: Evidence from Bidomain Simulations and Optical Mapping

Entcheva, Emilia; Eason, James; Efimov, Igor R.; Cheng, Yuanna; Malkin, R.A.; Claydon, F.J.

doi:10.1111/j.1540-8167.1998.tb00135.x

Cited by 71 publications

(37 citation statements)

References 30 publications

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“…30 Therefore, the 2-dimensional mapping technique used in this study provides somewhat limited insights into the mechanism. For instance, the driving force may come from deeper layers of the myocardium, which may introduce a distortion in the spatial correlation between postshock transmembrane polarizations and resulting propagation.…”

Section: Study Limitationsmentioning

confidence: 99%

Virtual Electrode–Induced Reexcitation

Cheng

Mowrey

Wagoner

et al. 1999

Circulation Research

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108

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Abstract-Mechanisms of defibrillation remain poorly understood. Defibrillation success depends on the elimination of fibrillation without shock-induced arrhythmogenesis. We optically mapped selected epicardial regions of rabbit hearts (nϭ20) during shocks applied with the use of implantable defibrillator electrodes during the refractory period. Monophasic shocks resulted in virtual electrode polarization (VEP). Positive values of VEP resulted in a prolongation of the action potential duration, whereas negative polarization shortened the action potential duration, resulting in partial or complete recovery of the excitability. After a shock, new propagated wavefronts emerged at the boundary between the 2 regions and reexcited negatively polarized regions. Conduction velocity and maximum action potential upstroke rate of rise dV/dt max of shock-induced activation depended on the transmembrane potential at the end of the shock. Linear regression analysis showed that dV/dt max of postshock activation reached 50% of that of normal action potential at a V m value of Ϫ56.7Ϯ0.6 mV postshock voltage (nϭ9257). Less negative potentials resulted in slow conduction and blocks, whereas more negative potentials resulted in faster conduction. Although wavebreaks were produced in either condition, they degenerated into arrhythmias only when conduction was slow. Shock-induced VEP is essential in extinguishing fibrillation but can reinduce arrhythmias by producing excitable gaps. Reexcitation of these gaps through progressive increase in shock strength may provide the basis for the lower and upper limits of vulnerability. The former may correspond to the origination of slow wavefronts of reexcitation and phase singularities. The latter corresponds to fast conduction during which wavebreaks no longer produce sustained arrhythmias. (Circ Res. 1999;85:1056-1066.)

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Section: Study Limitationsmentioning

confidence: 99%

Virtual Electrode–Induced Reexcitation

Cheng

Mowrey

Wagoner

et al. 1999

Circulation Research

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108

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“…Because of the frame rate of our camera and the defibrillation waveform duration, we were not able to determine the pattern of the change in transmembrane potential caused by the shocks. Although there are no data regarding these patterns in large hearts, results from rabbit hearts and computer simulations suggest that the medium surrounding the heart plays an important role 19 and that biphasic waveforms may act to homogenize shock-induced polarization. 3 We also did not attempt to quantify the small, locally propagating activation that has been reported to occur quickly after the shock.…”

Section: Limitationsmentioning

confidence: 99%

Mechanism of Ventricular Defibrillation for Near-Defibrillation Threshold Shocks

et al. 2001

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Background-To study the mechanism by which shocks succeed (SDF) or fail (FDF) to defibrillate, global cardiac activation and recovery and their relationship to defibrillation outcome were investigated for shock strengths with approximately equal SDF and FDF outcomes (DFT 50 ). Methods and Results-In 6 isolated pig hearts, dual-camera video imaging was used to record optically from Ϸ8000 sites on the anterior and posterior ventricular surfaces before and after 10 DFT 50 biphasic shocks. The interval between the shock and the last ventricular fibrillation activation preceding the shock (coupling interval, CI) and the time from shock onset to 90% repolarization of the immediate postshock action potential (RT 90 ) were determined at all sites. Of 60 shocks, 31 were SDF. The CI (59Ϯ7 versus 52Ϯ6 ms) and RT 90 (108Ϯ19 versus 88Ϯ8 ms) were significantly longer for SDF than FDF episodes. Spatial dispersions of CI (36Ϯ5 versus 34Ϯ3 ms) and RT 90 (40Ϯ16 versus 40Ϯ8 ms) were not significantly different for SDF versus FDF episodes. The first global activation cycle appeared focally on the left ventricular apical epicardium 78Ϯ32 ms after the shock. Conclusions-For near-threshold shocks, defibrillation outcome correlates with the electrical state of the heart at the time of the shock and on RT. Global dispersion of RT was similar in both SDF and FDF episodes, suggesting that it is not crucial in determining defibrillation outcome after DFT 50 shocks.

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“…Optical recordings often are distorted due to depth averaging. Therefore, the observed phenomenon could be explained by averaging of superficial regions of virtual cathode and a slightly deeper region of virtual anode, which could come close in the z-direction due to the rotation of fiber orientation (9). To rule out this hypothesis, we conducted numerical simulations in an active two-dimensional bidomain model.…”

Section: Origin Of Wavefront Of Activation During Unipolar Stimulationmentioning

confidence: 99%

Mechanisms of make and break excitation revisited: paradoxical break excitation during diastolic stimulation

Nikolski

Sambelashvili

Efimov

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Nikolski, Vladimir P., Aleksandre T. Sambelashvili, and Igor R. Efimov. Mechanisms of make and break excitation revisited: paradoxical break excitation during diastolic stimulation. Am J Physiol Heart Circ Physiol 282: H565-H575, 2002; 10.1152/ajpheart.00544.2001. Onset and termination of electric stimulation may result in "make" and "break" excitation of the heart tissue. Wikswo et al. (30) explained both types of stimulations by virtual electrode polarization. Make excitation propagates from depolarized regions (virtual cathodes). Break excitation propagates from hyperpolarized regions (virtual anodes). However, these studies were limited to strong stimulus intensities. We examined excitation during weak near-threshold diastolic stimulation. We optically mapped electrical activity from a 4 ϫ 4-mm area of epicardium of Langendorff-perfused rabbit hearts (n ϭ 12) around the pacing electrode in the presence (n ϭ 12) and absence (n ϭ 2) of 15 mM 2,3-butanedione monoxime. Anodal and cathodal 2-ms stimuli of various intensities were applied. We imaged an excitation wavefront with 528-s resolution. We found that strong stimuli (ϫ5 threshold) result in make excitation, starting from the virtual cathodes. In contrast, near-threshold stimulation resulted in break excitation, originating from the virtual anodes. Characteristic biphasic upstrokes in the virtual cathode area were observed. Break and make excitation represent two extreme cases of near-threshold and far-above-threshold stimulations, respectively. Both mechanisms are likely to contribute during intermediate clinically relevant strengths. optical mapping; virtual electrode; pacing THE ABILITY OF ELECTRIC POINT STIMULATION to produce a response in excitable tissues (11, 28) and induce (12) or terminate (17) arrhythmia in the heart is well known. However, the exact mechanisms of electric stimulation have been obscure until the recent discovery of virtual electrode polarization (VEP) produced by point stimulation (13,15,24,30,31). It results in a characteristic "dogbone" pattern of positive and negative polarizations. These polarizations of opposite sign are thought to be induced by a so-called virtual cathode and virtual anode. These virtual electrodes represent the driving force, which can be mathematically expressed as an activating function (19,27), which is also referred to as secondary sources (10). The activating function is governed by two major parameters: the gradient of extracellular electric field and structural heterogeneity of the heart, contributing to the polarization of the cellular membrane during stimulus. Active ionic properties of the heart, particularly calcium channels, modulate these polarizations (2,18,20,22).Dekker (4) demonstrated that both the onset (make) and termination (break) of stimulation of appropriate intensity and duration could produce a propagated response. Roth (20) and Wikswo et al. (30) provided the first mechanistic explanation of the "make" and "break" stimulation based on the VEP phenomenon.According to their theory...

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Virtual Electrode Effects in Transvenous Defibrillation‐Modulation by Structure and Interface: Evidence from Bidomain Simulations and Optical Mapping

Abstract: The present study concludes that VEE are present in transvenous defibrillation. They are shaped by the combined effect of cardiac tissue characteristics and interface conditions. Because of their size, VEE might contribute significantly to defibrillation outcome.

Cited by 71 publications

References 30 publications

Virtual Electrode–Induced Reexcitation

Virtual Electrode–Induced Reexcitation

Mechanism of Ventricular Defibrillation for Near-Defibrillation Threshold Shocks

Mechanisms of make and break excitation revisited: paradoxical break excitation during diastolic stimulation

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