The Strength-Interval Curve in Cardiac Tissue

Kandel, Sunil M.; Roth, Bradley J.

doi:10.1155/2013/134163

Cited by 12 publications

(23 citation statements)

References 54 publications

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“…This finding may underlie previous suggestions of the importance of vessels in secondary source formation [4]; however, given the relatively higher field strengths required for break excitation formation [28, 29], such a vessel-mediated mechanism may only be of significance during stronger (conventional) defibrillation protocols, and less so during low voltage protocols.…”

Section: Discussionsupporting

confidence: 68%

“…Our analysis suggests that vessels may still play an important role in low-energy defibrillation due to the close proximity of de- and hyper-polarised regions around the vessel, which we have shown is augmented by the presence of the vessel wall. Such proximity of regions of opposite polarity may facilitate break excitations, similar to the mechanism for unipolar stimulation [28, 29], allowing vessels to capture intramural tissue that is relatively refractory.…”

Section: Discussionmentioning

confidence: 99%

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Virtual electrodes around anatomical structures and their roles in defibrillation

2017

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BackgroundVirtual electrodes from structural/conductivity heterogeneities are known to elicit wavefront propagation, upon field-stimulation, and are thought to be important for defibrillation. In this work we investigate how the constitutive and geometrical parameters associated with such anatomical heterogeneities, represented by endo/epicardial surfaces and intramural surfaces in the form of blood-vessels, affect the virtual electrode patterns produced.Methods and resultsThe steady-state bidomain model is used to obtain, using analytical and numerical methods, the virtual electrode patterns created around idealized endocardial trabeculations and blood-vessels. The virtual electrode pattern around blood-vessels is shown to be composed of two dominant effects; current traversing the vessel surface and conductivity heterogeneity from the fibre-architecture. The relative magnitudes of these two effects explain the swapping of the virtual electrode polarity observed, as a function of the vessel radius, and aid in the understanding of the virtual electrode patterns predicted by numerical bidomain modelling. The relatively high conductivity of blood, compared to myocardium, is shown to cause stronger depolarizations in the endocardial trabeculae grooves than the protrusions.ConclusionsThe results provide additional quantitative understanding of the virtual electrodes produced by small-scale ventricular anatomy, and highlight the importance of faithfully representing the physiology and the physics in the context of computational modelling of field stimulation.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Virtual electrodes around anatomical structures and their roles in defibrillation

2017

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“…8 The first is electrotonic interaction of adjacent regions of depolarization and hyperpolarization. Dekker 3 identified four mechanisms of excitation: cathode make, cathode break, anode make, and anode break.…”

Section: Introductionmentioning

confidence: 99%

Intracellular Calcium and the Mechanism of the Dip in the Anodal Strength-Interval Curve in Cardiac Tissue

Kandel

Roth

2014

Circ J

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Background The strength-interval (SI) curve is an important measure of refractoriness in cardiac tissue. The anodal SI curve contains a “dip” in which the S2 threshold increases with interval. Two explanations exist for this dip: 1) electrotonic interaction between regions of depolarization and hyperpolarization, 2) the sodium-calcium exchange (NCX) current. The goal of this study is to use mathematical modeling to determine which explanation is correct. Methods and Results The bidomain model represents cardiac tissue and the Luo-Rudy model describes the active membrane. The SI curve is determined by applying a threshold stimulus at different time intervals after a previous action potential. During space-clamped and equal-anisotropy-ratios simulations, anodal excitation does not occur. During unequal-anisotropy-ratios simulations, following the S2 stimulus electrotonic currents, not membrane currents, are present during the few milliseconds before excitation. The dip disappears with no NCX current, but is present with 50% and 75% reduction of it. The calcium-induced-calcium-release (CICR) current has little effect on the dip. Conclusions These results indicate that neither NCX nor CICR current is responsible for the dip in the anodal SI curve. It is caused by the electrotonic interaction between regions of depolarization and hyperpolarization following the S2 stimulus.

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“…Computational bidomain simulations and experimental optical mapping experiments have shown agreement with predictions of SI curves for different polarities of applied stimulus (anodal or cathodal) (Kandel and Roth, 2013). SI curves are produced by applying a premature S 2 stimulus of a known strength to the tissue at a given instant of refractoriness, i.e., at a specific time following the S 1 paced beat.…”

Section: Methodsmentioning

confidence: 62%

“…The mechanisms by which relatively refractory cardiac tissue may be re-excited by a premature unipolar stimulus has been investigated in detail both in computational bidomain studies (Bray and Roth, 1997; Kandel and Roth, 2013, 2014) and corresponding optical mapping experimental work (Sidorov et al, 2005). These studies have demonstrated that the application of a unipolar stimulus to cardiac tissue induces a characteristic dog-bone VE pattern, consisting of neighboring de/hyperpolarization.…”

Section: Methodsmentioning

confidence: 99%

Bidomain Predictions of Virtual Electrode-Induced Make and Break Excitations around Blood Vessels

Connolly

Vigmond

Bishop

2017

Front. Bioeng. Biotechnol.

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Introduction and backgroundVirtual electrodes formed by field stimulation during defibrillation of cardiac tissue play an important role in eliciting activations. It has been suggested that the coronary vasculature is an important source of virtual electrodes, especially during low-energy defibrillation. This work aims to further the understanding of how virtual electrodes from the coronary vasculature influence defibrillation outcomes.MethodsUsing the bidomain model, we investigated how field stimulation elicited activations from virtual electrodes around idealized intramural blood vessels. Strength–interval curves, which quantify the stimulus strength required to elicit wavefront propagation from the vessels at different states of tissue refractoriness, were computed for each idealized geometry.ResultsMake excitations occurred at late diastolic intervals, originating from regions of depolarization around the vessel. Break excitations occurred at early diastolic intervals, whereby the vessels were able to excite surrounding refractory tissue due to the local restoration of excitability by virtual electrode-induced hyperpolarizations. Overall, strength–interval curves had similar morphologies and underlying excitation mechanisms compared with previous experimental and numerical unipolar stimulation studies of cardiac tissue. Including the presence of the vessel wall increased the field strength required for make excitations but decreased the field strength required for break excitations, and the field strength at which break excitations occurred was generally greater than 5 V/cm. Finally, in a more realistic ventricular slice geometry, the proximity of virtual electrodes around subepicardial vessels was seen to cause break excitations in the form of propagating unstable wavelets to the subepicardial layer.ConclusionRepresenting the blood vessel wall microstructure in computational bidomain models of defibrillation is recommended as it significantly alters the electrophysiological response of the vessel to field stimulation. Although vessels may facilitate excitation of relatively refractory tissue via break excitations, the field strength required for this is generally greater than those used in the literature on low-energy defibrillation. However, the high-intensity shocks used in standard defibrillation may elicit break excitation propagation from the coronary vasculature.

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The Strength-Interval Curve in Cardiac Tissue

Cited by 12 publications

References 54 publications

Virtual electrodes around anatomical structures and their roles in defibrillation

Virtual electrodes around anatomical structures and their roles in defibrillation

Intracellular Calcium and the Mechanism of the Dip in the Anodal Strength-Interval Curve in Cardiac Tissue

Bidomain Predictions of Virtual Electrode-Induced Make and Break Excitations around Blood Vessels

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