Bipolar stimulation of a three-dimensional bidomain incorporating rotational anisotropy

Muzikant, Adam L.; Henriquez, Craig S.

doi:10.1109/10.664201

Cited by 35 publications

(20 citation statements)

References 30 publications

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“…This method has been shown to be at least as accurate as histological studies in previous experiments (12,25,31) and computer simulations (7,21). Limitations of this method include assessing the fiber direction too long after stimulation so that encountered fiber rotation begins to modify the orientation of the maxima or poor quality of the signals masking the true center of the maxima.…”

Section: Data Acquisition Analysis and Displaymentioning

confidence: 99%

Epicardial and intramural excitation during ventricular pacing: effect of myocardial structure

Taccardi

Punske²,

Macchi

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Taccardi B, Punske BB, Macchi E, MacLeod RS, Ershler PR. Epicardial and intramural excitation during ventricular pacing: effect of myocardial structure. Am J Physiol Heart Circ Physiol 294: H1753-H1766, 2008. First published February 8, 2008 doi:10.1152/ajpheart.01400.2007.-Published studies show that ventricular pacing in canine hearts produces three distinct patterns of epicardial excitation: elliptical isochrones near an epicardial pacing site, with asymmetric bulges; areas with high propagation velocity, up to 2 or 3 m/s and numerous breakthrough sites; and lower velocity areas (Ͻ1 m/s), where excitation moves across the epicardial projection of the septum. With increasing pacing depth, the magnitude of epicardial potential maxima becomes asymmetric. The electrophysiological mechanisms that generate the distinct patterns have not been fully elucidated. In this study, we investigated those mechanisms experimentally. Under pentobarbital anesthesia, epicardial and intramural excitation isochrone and potential maps have been recorded from 22 exposed or isolated dog hearts, by means of epicardial electrode arrays and transmural plunge electrodes. In five experiments, a ventricular cavity was perfused with diluted Lugol solution. The epicardial bulges result from electrotonic attraction from the helically shaped subepicardial portions of the wave front. The highvelocity patterns and the associated multiple breakthroughs are due to involvement of the Purkinje network. The low velocity at the septum crossing is due to the missing Purkinje involvement in that area. The asymmetric magnitude of the epicardial potential maxima and the shift of the breakthrough sites provoked by deep stimulation are a consequence of the epi-endocardial obliqueness of the intramural fibers. These results improve our understanding of intramural and epicardial propagation during premature ventricular contractions and paced beats. This can be useful for interpreting epicardial maps recorded at surgery or inversely computed from body surface ECGs. propagation patterns; excitation mapping KNOWLEDGE OF THE MECHANISMS that govern the spread of excitation in the heart is a necessary prerequisite for understanding and interpreting abnormal sequences that occur in conduction disturbances, cardiac arrhythmias, localized ischemia, and myocardial infarctions. With the recent advancements in cardiac resynchronization therapy and other pacing strategies (15,35), it is even more relevant to better understand the spread of excitation during paced ventricular beats, as affected by the architecture of myocardial fibers and their anisotropic electrical properties.Experimental data published during the last 20 years show that epicardial and intramural ventricular pacing in canine hearts result in complex patterns of epicardial excitation, with multiple distinct areas of relatively slow and fast propagation (2,4,12,23,30,32). Published computer simulations of the spread of excitation in the ventricles, mostly based on eiconal equations, propose possible elect...

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Section: Data Acquisition Analysis and Displaymentioning

confidence: 99%

Epicardial and intramural excitation during ventricular pacing: effect of myocardial structure

Taccardi

Punske²,

Macchi

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…It is commonly assumed that propagation proceeds with equal velocity in all directions transverse to the myofiber axis. 11,12 This notion of transverse electrical isotropy is at odds with recent descriptions of myocardial structure. It has been proposed that the sheet structure of myocardium may lead to orthogonal anisotropy with electrical propagation across muscle layers slower than propagation transverse to the myofiber axis within layers.…”

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confidence: 99%

Cardiac Microstructure

Hooks

Tomlinson

Marsden

et al. 2002

Circulation Research

223

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Abstract-Our understanding of the electrophysiological properties of the heart is incomplete. We have investigated two issues that are fundamental to advancing that understanding. First, there has been widespread debate over the mechanisms by which an externally applied shock can influence a sufficient volume of heart tissue to terminate cardiac fibrillation. Second, it has been uncertain whether cardiac tissue should be viewed as an electrically orthotropic structure, or whether its electrical properties are, in fact, isotropic in the plane orthogonal to myofiber direction. In the present study, a computer model that incorporates a detailed three-dimensional representation of cardiac muscular architecture is used to investigate these issues. We describe a bidomain model of electrical propagation solved in a discontinuous domain that accurately represents the microstructure of a transmural block of rat left ventricle. From analysis of the model results, we conclude that (1) the laminar organization of myocytes determines unique electrical properties in three microstructurally defined directions at any point in the ventricular wall of the heart, and (2)

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“…They found that excitation arises from the depolarized region of tissue, and occurs for both cathodal and anodal stimulation. Muzikant and Henriquez [26][27][28] extended this model to include the rotating fiber direction across the heart wall. For large electrodes, the distribution of depolarization and hyperpolarization is modified [29], with strongest depolarization under the edge of the cathode [30].…”

Section: Unipolar Stimulationmentioning

confidence: 99%

Numerical Simulations of Cardiac Tissue Excitation and Pacing Using the Bidomain Model

Roth¹

2011

TOPETJ

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Abstract:The last two decades have produced significant advances in our theoretical understanding of cardiac pacing. The bidomain model, a mathematical representation of the anisotropic electrical properties of cardiac tissue, has provided insight into many long-standing mysteries of pacing, such as the mechanisms of make and break excitation, the shape of the strength-interval curve, and the induction of reentry by burst pacing. This paper reviews the application of the bidomain model to these and other topics, and summarizes our theoretical understanding of how electrical excitation of the heart works.

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Bipolar stimulation of a three-dimensional bidomain incorporating rotational anisotropy

Cited by 35 publications

References 30 publications

Epicardial and intramural excitation during ventricular pacing: effect of myocardial structure

Epicardial and intramural excitation during ventricular pacing: effect of myocardial structure

Cardiac Microstructure

Numerical Simulations of Cardiac Tissue Excitation and Pacing Using the Bidomain Model

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