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Natalia A Trayanova

Publications and source records attributed to Natalia A Trayanova.

13 recordsLinked to original sources
PubMed2006

Mechanistic enquiry into the effect of increased pacing rate on the upper limit of vulnerability.

The goal of this study is to investigate the mechanisms responsible for the increase in the upper limit of vulnerability (ULV; highest shock strength that induces arrhythmia) following the increase in pacing rate. To accomplish this goal, the study employs a three-dimensional bidomain finite element model of a slice through the canine ventricles. The preparation was paced eight times at a basic cycle length (BCL) of either 80 or 150ms followed by delivery of shocks of various strengths and timings. Our results demonstrate that the shock strength, which induced an arrhythmia 50% of the time, increased 20% for the faster pacing compared to the slower pacing. Analysis of the mechanisms underlying the increased vulnerability revealed that delayed post-shock activations originating in the tissue depths appear as breakthrough activations on the surfaces of the preparation following an isoelectric window (IW). However, the IW duration was consistently shorter in the faster-paced preparation. Consequently, breakthrough activations appeared on the surfaces of this preparation earlier, when the tissue was less recovered, resulting in higher probability of unidirectional block and reentry. This explains why shocks of the same strength were more likely to result in arrhythmia induction when delivered to a preparation that was rapidly paced.

Action Potentials↗
PubMed2006

Action potential morphology heterogeneity in the atrium and its effect on atrial reentry: a two-dimensional and quasi-three-dimensional study.

Atrial fibrillation (AF) is believed to be perpetuated by recirculating spiral waves. Atrial structures are often characterized with action potentials of varying morphologies; however, the role of the structure-dependent atrial electrophysiological heterogeneity in spiral wave behaviour is not well understood. The purpose of this study is to determine the effect of action potential morphology heterogeneity associated with the major atrial structures in spiral wave maintenance. The present study also focuses on how this effect is further modulated by the presence of the inherent periodicity in atrial structure. The goals of the study are achieved through the simulation of electrical behaviour in a two-dimensional atrial tissue model that incorporates the representation of action potentials in various structurally distinct regions in the right atrium. Periodic boundary conditions are then imposed to form a cylinder (quasi three-dimensional), thus allowing exploration of the additional effect of structure periodicity on spiral wave behaviour. Transmembrane potential maps and phase singularity traces are analysed to determine effects on spiral wave behaviour. Results demonstrate that the prolonged refractoriness of the crista terminalis (CT) affects the pattern of spiral wave reentry, while the variation in action potential morphology of the other structures does not. The CT anchors the spiral waves, preventing them from drifting away. Spiral wave dynamics is altered when the ends of the sheet are spliced together to form a cylinder. The main effect of the continuous surface is the generation of secondary spiral waves which influences the primary rotors. The interaction of the primary and secondary spiral waves decreased as cylinder diameter increased.

Action Potentials↗
PubMed2006

Characterization of the relationship between preshock state and virtual electrode polarization-induced propagated graded responses resulting in arrhythmia induction.

BACKGROUND: Studies have demonstrated that failed defibrillation shocks often are followed by an electrically quiescent period (isoelectric window); however, the underlying mechanisms remain incompletely understood. We recently suggested a new mechanism termed "virtual electrode polarization-induced propagated graded responses" (VEPiPGRs) that might play a role in the origin of the global postshock activation following the isoelectric window. OBJECTIVES: The purpose of this study to elucidate the circumstances under which VEPiPGR activations originate for shocks given to paced right ventricular preparations. Specifically, we examined the dependence of VEPiPGRs on coupling interval (CI) and shock polarity and whether VEPiPGRs emerge preferentially on the epicardium or the endocardium. METHODS: Simultaneous endocardial and epicardial activity in isolated right ventricular preparations (n = 4) was imaged optically following shocks of strength +/-5A. All VEPiPGRs were analyzed, and the time T from shock end to activation onset was recorded (isoelectric window is the smallest T among activations that propagated globally). RESULTS: VEPiPGR activations occurred for CIs in the range from 80 to 150 ms. Average duration of T was 64.5 +/- 18.15 ms, with T decreasing as CI increased (Tmax = 82 ms, Tmin = 46 ms, linear-fit slope = -0.675). The average earliest CI at which cathodal (+5A) shocks resulted in VEPiPGRs was 87 ms compared with 116 ms for anodal (-5A) shocks. All VEPiPGR activations emerged first on the epicardium in a focal pattern, and all induced ventricular fibrillation. CONCLUSION: The global activation that terminates the isoelectric window could result from VEPiPGRs that find an exit pathway. VEPiPGRs originate at the sites of maximum action potential abbreviation by the shock, always on the epicardium for the preparation used here.

Action Potentials↗
PubMed2006

Cardiac defibrillation and the role of mechanoelectric feedback in postshock arrhythmogenesis.

Ventricular dilatation increases the defibrillation threshold (DFT). In order to elucidate the mechanisms responsible for this increase, the present article investigates changes in the postshock behavior of the myocardium upon stretch. A two-dimensional electro-mechanical model of cardiac tissue incorporating heterogeneous fiber orientation was used to explore the effect of sustained stretch on postshock behavior via (a) recruitment of mechanosensitive channels (MSC) and (b) tissue deformation and concomitant changes in tissue conductivities. Recruitment of MSC had no influence on vulnerability to electric shocks as compared to control, but increased the complexity of postshock VF patterns. Stretch-induced deformation and changes in tissue conductivities resulted in a decrease in vulnerability to electric shocks.

Arrhythmias, Cardiac↗
PubMed2005

Differences between left and right ventricular chamber geometry affect cardiac vulnerability to electric shocks.

Although effects of shock strength and waveform on cardiac vulnerability to electric shocks have been extensively documented, the contribution of ventricular anatomy to shock-induced polarization and postshock propagation and thus, to shock outcome, has never been quantified; this is caused by lack of experimental methodology capable of mapping 3-D electrical activity. The goal of this study was to use optical imaging experiments and 3-D bidomain simulations to investigate the role of structural differences between left and right ventricles in vulnerability to electric shocks in rabbit hearts. The ventricles were paced apically, and uniform-field, truncated-exponential, monophasic shocks of reversed polarity were applied over a range of coupling intervals (CIs) in experiment and model. Experiments and simulations revealed that reversing the direction of externally-applied field (RV- or LV- shocks) alters the shape of the vulnerability area (VA), the 2-D grid encompassing episodes of arrhythmia induction. For RV- shocks, VA was nearly rectangular indicating little dependence of postshock arrhythmogenesis on CI. For LV- shocks, the probability of arrhythmia induction was higher for longer than for shorter CIs. The 3-D simulations demonstrated that these effects stem from the fact that reversal of field direction results in relocation of the main postshock excitable area from LV wall (RV- shocks) to septum (LV- shocks). Furthermore, the effect of septal (but not LV) excitable area in postshock propagation was found to strongly depend on preshock state. Knowledge regarding the location of the main postshock excitable area within the 3-D ventricular volume could be important for improving defibrillation efficacy.

Animals↗
PubMed2005

Cell and tissue responses to electric shocks.

AIM: Existing models of myocardial membrane kinetics have not been able to reproduce the experimentally-observed negative bias in the asymmetry of transmembrane potential changes (DeltaV(m)) induced by strong electric shocks. The goals of this study are (1) to demonstrate that this negative bias could be reproduced by the addition, to the membrane model, of electroporation and an outward current, I(a), part of the K(+) flow through the L-type Ca(2+)-channel, and (2) to determine how such modifications in the membrane model affect shock-induced break excitation in a 2D preparation. METHODS AND RESULTS: We conducted simulations of shocks in bidomain fibres and sheets with membrane dynamics represented by the Luo-Rudy dynamic model (LRd'2000), to which electroporation (LRd + EP model) and the outward current, I(a), activated upon strong shock-induced depolarization (aLRd model) was added. Assuming I(a) is a part of K(+) flow through the L-type Ca(2+)-channel enabled us to reproduce both the experimentally observed rectangularly-shaped positive DeltaV(m) and the value of near 2 of the negative-to-positive DeltaV(m) ratio. In the sheet, I(a) not only contributed to the negative bias in DeltaV(m) asymmetry at sites polarized by physical and virtual electrodes, but also restricted positive DeltaV(m). Electroporation, in its turn, was responsible for the decrease in cathode-break excitation threshold in the aLRd sheet, compared with the other two cases, as well as for the occurrence of the excitation after the shock-end rather than during the shock. CONCLUSIONS: The incorporation of electroporation and I(a) in a membrane model ensures match between simulation results and experimental data. The use of the aLRd model results in a lower threshold for shock-induced break excitation.

Animals↗
PubMed2004

Asymmetry in membrane responses to electric shocks: insights from bidomain simulations.

Models of myocardial membrane dynamics have not been able to reproduce the experimentally observed negative bias in the asymmetry of transmembrane potential changes (DeltaVm) induced by strong electric shocks delivered during the action potential plateau. The goal of this study is to determine what membrane model modifications can bridge this gap between simulation and experiment. We conducted simulations of shocks in bidomain fibers and sheets with membrane dynamics represented by the LRd'2000 model. We found that in the fiber, the negative bias in DeltaVm asymmetry could not be reproduced by addition of electroporation only, but by further addition of hypothetical outward current, Ia, activated upon strong shock-induced depolarization. Furthermore, the experimentally observed rectangularly shaped positive DeltaVm, negative-to-positive DeltaVm ratio (asymmetry ratio) = approximately 2, electroporation occurring at the anode only, and the increase in positive DeltaVm caused by L-type Ca2+-channel blockade were reproduced in the strand only if Ia was assumed to be a part of K+ flow through the L-type Ca2+-channel. In the sheet, Ia not only contributed to the negative bias in DeltaVm asymmetry at sites polarized by physical and virtual electrodes, but also restricted positive DeltaVm. Inclusion of Ia and electroporation is thus the bridge between experiment and simulation.

Action Potentials↗
PubMed2003

Mechanistic inquiry into decrease in probability of defibrillation success with increase in complexity of preshock reentrant activity.

Energy requirements for successful antiarrhythmia shocks are arrhythmia specific. However, it remains unclear why the probability of shock success decreases with increasing arrhythmia complexity. The goal of this research was to determine whether a diminished probability of shock success results from an increased number of functional reentrant circuits in the myocardium, and if so, to identify the responsible mechanisms. To achieve this goal, we assessed shock efficacy in a bidomain defibrillation model of a 4-mm-thick slice of canine ventricles. Shocks were applied between a right ventricular cathode and a distant anode to terminate either a single scroll wave (SSW) or multiple scroll waves (MSWs). From the 160 simulations conducted, dose-response curves were constructed for shocks given to SSWs and MSWs. The shock strength that yielded a 50% probability of success (ED(50)) for SSWs was found to be 13% less than that for MSWs, which indicates that a larger number of functional reentries results in an increased defibrillation threshold. The results also demonstrate that an isoelectric window exists after both failed and successful shocks; however, shocks of strength near the ED(50) value that were given to SSWs resulted in 16.3% longer isoelectric window durations than the same shocks delivered to MSWs. Mechanistic inquiry into these findings reveals that the two main factors underlying the observed relationships are 1) smaller virtual electrode polarizations in the tissue depth, and 2) differences in preshock tissue state. As a result of these factors, intramural excitable pathways leading to delayed breakthrough on the surface were formed earlier after shocks given to MSWs compared with SSWs and thus resulted in a lower defibrillation threshold for shocks given to SSWs.

Animals↗
PubMed2003

Postshock arrhythmogenesis in a slice of the canine heart.

INTRODUCTION: Recent evidence has demonstrated that defibrillation shocks terminate or reset reentrant activity in the myocardium through the generation of virtual electrode polarization (VEP). Previous research has revealed that the shock establishes phase singularities (PSs) in the tissue via the VEP mechanism. The aim of this study was to examine, as a function of shock strength and electrode configuration, the relationship between end-shock PSs and the reentrant circuits established after failed defibrillation attempts. METHODS AND RESULTS: The study uses a complex three-dimensional finite-element bidomain model of a slice of the canine heart characterized by realistic geometry and fiber architecture and undergoing a single scroll wave. Defibrillation shocks of increasing strength are delivered through three different electrode configurations. The results demonstrated that >98% of all PSs have a lifetime of half a reentrant cycle or less. Stronger shocks result in a faster rate of annihilation of postshock PSs. For failed shocks, the surviving PSs underlie the activity of one or more scroll waves, which remain stationary in the slice. For all electrode configurations tested, the increase in shock strength leads to a rapid initial increase in the number of postshock reentries followed by a slower decrease; similar behavior is observed with regard to end-shock PSs. CONCLUSION: These results present new evidence regarding the mechanisms underlying failure of defibrillation shocks.

Animals↗
PubMed2002

Termination of reentry by a long-lasting AC shock in a slice of canine heart: a computational study.

INTRODUCTION: A heart in fibrillation can be entrained by long-lasting alternating current (AC) stimuli, leading to defibrillation. To investigate the role entrainment plays in defibrillation, computer simulations of AC cardioversion in a three-dimensional slice of the canine heart were performed. METHODS AND RESULTS: A bidomain finite element model of a 1-mm thick slice across the ventricles of a canine heart was used to simulate termination of transmural reentry with AC shocks. Cardioversion defibrillation thresholds (DFTs) were determined for 200-msec (L) AC shocks at varying frequencies. At the DFT, the entire tissue is entrained by the AC shock. DFT decreases as the frequency of the long-lasting AC shock increases. We hypothesize that this decrease is due to the short period of the high-frequency AC waveform, leaving strong virtual electrode polarization (VEP) after the shock ends. To test this hypothesis, the end-shock VEP were compared for different frequencies, demonstrating stronger polarization as frequency increased. To examine whether entrainment by the long-lasting AC shock contributes to the VEP at the end of the shock, additional simulations were conducted using single-period (Z) AC waveforms. Z waveform DFTs were higher than L waveform DFTs; the Z waveform VEP was weaker than the L waveform VEP at the same frequency. This indicates that entrainment contributes to the development of stronger VEP and, thus, to lower DFT at high frequencies. CONCLUSION: This study offers for the first time a mechanistic insight into cardioversion with long-lasting AC shocks.

Animals↗
PubMed2002

Computational techniques for solving the bidomain equations in three dimensions.

The bidomain equations are the most complete description of cardiac electrical activity. Their numerical solution is, however, computationally demanding, especially in three dimensions, because of the fine temporal and spatial sampling required. This paper methodically examines computational performance when solving the bidomain equations. Several techniques to speed up this computation are examined in this paper. The first step was to recast the equations into a parabolic part and an elliptic part. The parabolic part was solved by either the finite-element method (FEM) or the interconnected cable model model (ICCM). The elliptic equation was solved by FEM on a coarser grid than the parabolic problem and at a reduced frequency. The performance of iterative and direct linear equation system solvers was analyzed as well as the scalability and parallelizability of each method. Results indicate that the ICCM was twice as fast as the FEM for solving the parabolic problem, but when the total problem was considered, this resulted in only a 20% decrease in computation time. The elliptic problem could be solved on a coarser grid at one-quarter of the frequency at which the parabolic problem was solved and still maintain reasonable accuracy. Direct methods were faster than iterative methods by at least 50% when a good estimate of the extracellular potential was required. Parallelization over four processors was efficient only when the model comprised at least 500,000 nodes. Thus, it was possible to speed up solution of the bidomain equations by an order of magnitude with a slight decrease in accuracy.

Algorithms↗